Clinical Dermatology Pocket Guide

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DERM Notes Dermatology Clinical Pocket Guide Benjamin Barankin, MD Anatoli Freiman, MD

Purchase additional copies of this book at your health science bookstore or directly from F. A. Davis by shopping online at www.fadavis.com or by calling 800-323-3555 (US) or 800-665-1148 (CAN) A Davis’s Notes Book

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F. A. Davis Company 1915 Arch Street Philadelphia, PA 19103 www.fadavis.com Copyright © 2006 by F. A. Davis Company All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without written permission from the publisher. Printed in China by Imago Last digit indicates print number: 10 9 8 7 6 5 4 3 2 1 Acquisitions Editor: Andy McPhee Developmental Editor: Melissa Reed Design Manager: Carolyn O’Brien Reviewers: Paul Arnstein, RN, PHD, FNP-C, APRN-BC, Robert T. Brodell, MD, Morton A. Diamond, MD, FACP, FACC, FAHA, David J. Elpern, MD, Henry Foong, MD, FRCP, MBBS, Susan S. Kelly-Weeder, PhD, APRN, BC, FND, Adam Kinninger, OMS III, EMT-B, BS, Daniel Loo, MD, Margaret McAllister, PhD, FNP, APRN, BC, FAANP, Andrei Metelitsa, MD, BMSC, Karima Miller, MSN, FNP-C, BSN, Gary Reiss, MD, MPH, MBA, Robert J. Spears, MPAS, PA-C, Debbie Sullivan, PhD, PA-C, Travis J. Widman, MD, Julie Zlotnick, Student As new scientific information becomes available through basic and clinical research, recommended treatments and drug therapies undergo changes. The author(s) and publisher have done everything possible to make this book accurate, up to date, and in accord with accepted standards at the time of publication. The author(s), editors, and publisher are not responsible for errors or omissions or for consequences from application of the book, and make no warranty, expressed or implied, in regard to the contents of the book. Any practice described in this book should be applied by the reader in accordance with professional standards of care used in regard to the unique circumstances that may apply in each situation. The reader is advised always to check product information (package inserts) for changes and new information regarding dose and contraindications before administering any drug. Caution is especially urged when using new or infrequently ordered drugs. Authorization to photocopy items for internal or personal use, or the internal or personal use of specific clients, is granted by F. A. Davis Company for users registered with the Copyright Clearance Center (CCC) Transactional Reporting Service, provided that the fee of $.10 per copy is paid directly to CCC, 222 Rosewood Drive, Danvers, MA 01923. For those organizations that have been granted a photocopy license by CCC, a separate system of payment has been arranged. The fee code for users of the Transactional Reporting Service is: 80361493-4/06 0 ⫹ $.10.

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BASIC

DX

TX

A-F

G-M

N-S

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TOOLS

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Look for our other Davis’s Notes titles Available Now!

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1 History Taking in Dermatology ID: Age, race, sex, occupation, hobbies HPI: a. b. c. d. e.

When did the rash/lesion start or was first noticed? Where did it start? Symptoms: E.g., does it itch, hurt, burn? Evolution: How has it spread or developed over time? What makes the rash or symptoms worse? E.g., heat, cold, sun, exercise, season f. What therapy has been tried?—dose, duration, frequency of actual use

Contacts (where appropriate): Pets or farm animal contact, travel, motel stays PMHx: Diabetes, hypertension, atopy (eczema, asthma, hay fever), previous skin cancers or other skin problems; STDs, HIV, blood transfusions Medications: Dosage listed for any derm drugs; specific topical steroid names Allergies (& specific reaction) Habits: Smoking, alcohol, drug abuse FamHx: Psoriasis, melanoma, atopy, genetic conditions (e.g., neurofibromatosis) Constitutional symptoms (if relevant: infection, previous malignancy): Headache, fever, chills, sweats, fatigue, weakness, anorexia, weight loss Review of systems: Based on clinical scenario. E.g., If autoimmune connective tissue disease is in the differential, ask about arthralgias, myalgias, aphthous ulcers, keratoconjunctivitis sicca, Raynaud’s phenomenon, neurologic or renal problems.

BASICS

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BASICS

Approach to Describing Skin Lesions Mnemonic: LES T. CABS

Descriptors Location & Distribution Symmetrical, asymmetrical, sun-exposed, flexures/extensors, acral (hands/feet) Erythema Erythematous or nonerythematous lesions &/or underlying skin Surface Features Crusting, rough, smooth, scaly, warty Type Cyst, macule, papule, pustule, ulcer, vesicle Color Blue, brown, pink, purple, red, white Arrangement Single or multiple, discrete, unilateral, generalized, disseminated, grouped, annular, gyrate, dermatomal, linear, serpiginous Border & Shape Well- or poorly defined, active edge, round, oval, irregular, pedunculated Special Sites/Systemic Scalp, mouth, nails, genitalia, systemic disease, constitutional symptoms

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3 Terminology of Dermatology Lesion Abscess

Annular

Definition

Examples

Accumulation of pus in the dermis or subcutaneous tissue Ring-shaped

Depressed surface due to a thinned epidermis and/or dermis and/or subcutis Bulla (blister) A large, circumscribed, fluid-containing elevation (⬎5 mm) Liner S-shaped Burrow elevated channel in the epidermis Inflammatory nodules Carbuncle or abscess of numerous contiguous hair follicles Plugged pilosebaceous Comedo follicle containing serum & keratin. Closed ⫽ whitehead; open ⫽ blackhead Dried serum, pus, or Crust (scab) blood (usually preceded by vesicle, bulla, or pustule) Nodule containing Cyst fluid, cells or keratin Atrophy

Perianal abscess, Staphylococcus aureus infection Granuloma annulare, tinea corporis Lichen sclerosus, necrobiosis lipoidica, prolonged potent topical steroid use Bullous impetigo, bullous pemphigoid, pemphigus vulgaris Scabies

Hidradenitis suppurativa

Acne

Herpes simplex or VZV, impetigo

Epidermoid cyst, mucous cyst, pilar cyst

(Continued text on following page)

BASICS

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BASICS

Terminology of Dermatology (Continued) Lesion Ecchymosis (“bruise”) Erosion

Erythema

Excoriation

Exudate

Fissure

Folliculitis Furuncle

Definition

Examples

Large, confluent area of purpura Partial loss of epidermis. Heals without scarring. Redness that blanches on pressure Shallow abrasion due to scratching. Linear or pinpoint erosions or crusts. Serum, blood, or pus accumulated on the skin surface Linear split in epidermis &/or crack in (skin) dermis Pustule involving a hair follicle Deep necrotizing type of folliculitis

Postsurgery or trauma Eczema, lichen simplex, pemphigus vulgaris Cellulitis, erysipelas, erythroderma, sunburn Dermatitis

Acute eczema

Eczema

Folliculitis due to S. aureus Furuncle due to S. aureus, hidradenitis suppurativa Actinic keratosis, corn, squamous cell carcinoma, wart

Rough, uneven surface due to accumulation of keratin. Hard to pick off, unlike crust. Lichenification Focal area of thickened Atopic dermatitis, lichen simplex skin with accentuachronicus tion of skin lines due to rubbing/scratching Keratin/horn


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5 Terminology of Dermatology (Continued) Lesion

Definition

Examples

Linear

Straight line

Livedo

Criss-cross pattern

Macule

Flat, circumscribed area of altered skin color ⬍1 cm Solid, round circumErythema nodosum, keratoscribed elevation ⬎5 acanthoma, prurigo nodumm laris, rheumatoid nodule Raised, solid lesion Acne, basal cell carcinoma, ⬍5 mm lichens planus, molluscum contagiosum, rosacea, skin tag, syringoma Flat, pigmented lesion Café au lait patch, melasma, ⬎5 mm Mongolian spot, nevus of Ota, port-wine stain, vitiligo Small, nonblanching, Capillaritis, meningored-brown macules coccemia A ⬎5-mm, flat-topped Giant hairy nevus, mycosis raised lesion (diafungoides, psoriasis, tinea meter ⬎ thickness) corporis Visible collection of Drug-eruption, Henochfree red blood cells Schönlein purpura (red, purple, brown); nonblanchable A small papule Acne, folliculitis, pustular containing pus psoriasis rosacea Fine lace pattern Oral lichen planus

Nodule

Papule

Patch

Petechia Plaque

Purpura

Pustule Reticulate

Allergic contact dermatitis (poison ivy), Koebner reaction to lichen planus or psoriasis Cutis marmorata, erythema ab igne, livedo reticularis Freckle, junctional nevus, lentigo, pityriasis versicolor, vitiligo


BASICS

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BASICS

Terminology of Dermatology (Continued) Lesion Scale

Definition

Examples

Serpiginous

Thick stratum corneum due to increased proliferation or cohesion of keratinocytes Healed dermal (or deeper) lesion following trauma/inflammation Skin induration/ hardening Snakelike appearance

Stellate

Star-shaped

Target lesions

Three zones: dark or blistered center surrounded by a second pale zone and a third zone of a rim of erythema Small, dilated superficial blood vessels Loss of tissue affecting the entire epidermis and part of the dermis. Surface exudate &/or crusting often present. Heals with scarring.

Scar (cicatrix) Sclerosis

Telangiectasia Ulcer

Umbilicated

Round depression in center of papule

Ichthyosis, psoriasis, seborrheic dermatitis, tinea capitis/corporis Acne scars, hypertrophic scars, keloids Morphea Cutaneous larva migrans, elastosis perforans serpiginosa Stellate pseudoscars on forearms after years of sun damage Erythema multiforme

Rosacea, steroid side effect Decubitus ulcer, pyoderma gangrenosum, venous (stasis) ulcer

Molluscum contagiosum, umbilicated vesicles of herpes


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7 Terminology of Dermatology (Continued) Lesion

Definition

Vesicle

Examples

Dermatitis herpetiformis, dyshidrotic eczema, hand-foot-and-mouth disease, herpes simplex, pemphigus vulgaris, VZV Nevus sebaceous, seborFinger-like projecrheic keratosis, warts tions on the surface Dermographism, urticaria, Transient swelling urticaria pigmentosa due to dermal edema; pruritic Epidermal nevi, inconSwirling pattern tinentia pigmenti (late) A small papule containing clear fluid

Warty/papillomatous Wheal (hive)

Whorled

Structure and Function of Skin Eccrine sweat duct

Dermal papillae

Dermal nerve fibers Hair follicle Sebaceous gland

Layers of Epidermis: Stratum corneum Stratum granulosum Stratum spinosum Stratum basale

Dermis

Deep arteriovenous plexus

BASICS

Subcutaneous Arrector Eccrine fat pili muscle sweat gland Pacinian corpuscle

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BASICS Three Layers of Skin 1. Epidermis: Keratinocytes, melanocytes, Langerhans cells, Merkel cells 2. Dermis: Collagen (types I & III), elastin, proteoglycans, hair follicles, glands (apocrine, eccrine, sebaceous), blood vessels, lymphatics, nerves 3. Subcutis (subcutaneous fat): Adipose tissue, large blood vessels, nerves

Epidermis: 4 Layers 1. 2. 3. 4.

Basal cell layer (stratum basalis) Spiny cell layer (stratum spinosum) Granular cell layer (stratum granulosum) Cornified layer (stratum corneum)

Dermis: 2 Layers 1. Papillary dermis (thin zone beneath epidermis) 2. Reticular dermis (bulk of dermis)

Special Tests and Procedures Special Tests & Procedures in Dermatology BIOPSIES OF SKIN Choice of technique depends on the pathology suspected 1. Shave biopsy: A superficial skin biopsy with a #10 or #15 blade. Useful for elevated lesions (e.g., benign compound nevi). No sutures; bleeding stopped by Monsel’s solution, aluminum chloride, or electrodessication.

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9 2. Punch biopsy: A round “cookie-cutter” knife that obtains tissue specimen. Usually 3 to 5 mm is taken. Usually 1 to 2 sutures are required.

3. Incisional biopsy (“wedge”): An elliptical partial removal of a lesion down to fat. Useful, for example, when a malignancy is too large to remove by simple surgery, in scleroderma, panniculitis, and pyoderma gangrenosum. Requires layered closure with sutures. 4. Excisional biopsy: An elliptical complete removal of lesion down to fat. Useful in completely removing skin cancers. Requires layered closure with sutures. 5. Curettage: For hyperkeratotic lesions (e.g., SK, warts, BCC); often accompanied by cautery. 6. Snip (scissors): Skin tags, filiform warts

BASICS

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WRONG

RIGHT Relaxed skin tension lines A

Margin of normal skin

x 1 < y 3 x

B 1

y

3

C

Epidermis D

Dermis Fat

Examples of excision ellipses on facial crease lines

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11 A biopsy is warranted in: 1. Skin neoplasms. 2. Bullous disorders (with immunofluorescence simultaneously). 3. Autoimmune connective tissue diseases—lupus, dermatomyositis. 4. Skin disorders in which clinical exam is insufficient for diagnosis. DERMOSCOPY A hand lens with built-in lighting and magnification (10–30X). It allows for the noninvasive inspection of deeper layers of the skin (dermal-epidermal junction and beyond). This is especially useful in distinguishing benign and malignant growth patterns in pigmented lesions.

DIASCOPY A microscope slide or magnifying glass is pressed against lesion. ■ Blanching: Dilated capillaries (erythema) ■ Nonblanching: Extravasated blood (purpura) ■ “Apple-jelly” color (yellow-brown): Granulomas as seen in sarcoidosis, necrobiosis lipoidica, tuberculosis of skin, and granuloma annulare

IMMUNOFLUORESCENCE Tissue is transported in liquid nitrogen or Michel’s media (most commonly). 1. Direct immunofluorescence (DIF): A histologic stain for antibodies or other tissue proteins. Useful in bullous pemphigoid, cicatricial pemphigoid, dermatitis herpetiformis, epidermolysis bullosa acquisita, HenochSchönlein purpura, herpes gestationis, linear IgA bullous disease, lupus erythematosus, and pemphigus

BASICS

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BASICS 2. Indirect immunofluorescence (IIF): Examines the presence of circulating autoantibodies in the serum. Can give titers that are useful in pemphigus and other diseases to determine disease activity. KOH (POTASSIUM HYDROXIDE) Scrape presumed dermatophyte infection with an alcohol pad or water and scrape with a #15 blade onto a slide. Then apply 2 drops of 10% to 20% KOH on slide to dissolve keratin for fungal elements. Heating accelerates the process. May have to wait several minutes to visualize. MAGNIFYING LENS Handheld magnifier or dermatoscope, or loupes, provide enhanced morphologic detail; should be carried around at all times. PATCH TESTING: The test of choice for diagnosing allergic contact dermatitis. Patch test allergens are usually purchased prepared, but can be prepared individually. Allergens are placed in special wells (e.g., Finn chambers®) and applied to the back for 48 hours using Scanpor tape® and then removed; they are interpreted at 48 hours after first application, and then again at 96 hours. Contact hypersensitivity will show as a papular-vesicular reaction.

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13 Patch testing methodology

A. Patch tests are prepared

B. Patches are affixed to upper back

C. Hypersensitivity is determined

BASICS

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BASICS ⫹/⫺ ⫹ ⫹⫹ ⫹⫹⫹ IRR ⫺ NT

⫽ Macular erythema only ⫽ Weak reaction: erythema, infiltration, papules (no vesicles) ⫽ Strong reaction: edema, vesiculation ⫽ Extreme reaction: spreading, bullous, ulcerative ⫽ Irritant morphologic appearance ⫽ Negative reaction ⫽ Not tested

TZANCK SMEAR Quickly diagnoses HSV and VZV (doesn’t distinguish between them). Scrape the base of an early blister, air dry or fix with ethanol, stain with Giemsa or Wright’s stain. Look for multinucleated giant cells or atypical keratinocytes with large nuclei. WOOD’S LAMP A 360-nm light source useful in localizing the site of melanin in Caucasian skin, diagnosing infections and porphyria. Specifically, it is useful in diagnosing disorders of pigmentation such as vitiligo; erythrasma; porphyria cutanea tarda; pseudomonas infection of the skin; tinea capitis; and tinea versicolor. ■ Dull yellow: Tinea versicolor ■ Yellow-green: Some Dermatophytes (esp. Microsporum species; audounii, canis, distortum, ferrugineum, gypseum, & T. schonleinii) ■ Coral red: Erythrasma ■ Pale blue-green: Pseudomonas ■ Dark pink urine: Porphyria cutanea tarda ■ Completely white: Vitiligo

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15 Dermatoses by Location FACE Acne Actinic keratosis Basal cell carcinoma Contact dermatitis Dermatomyositis Herpes simplex Impetigo Keratoacanthoma Lupus erythematosus Melasma Nevus Perioral dermatitis Rosacea Sarcoidosis Sebaceous hyperplasia Seborrheic dermatitis Seborrheic keratosis Squamous cell carcinoma Varicella-zoster infection Vitiligo

LIMBS Atopic eczema Bullous pemphigoid Cellulitis Dermatofibroma Erythema multiforme Granuloma annulare Henoch-Schönlein purpura Keratosis pilaris Lichen planus Melanoma Nevus Psoriasis Pyoderma gangrenosum Seborrheic keratosis Stasis dermatitis Ulcer Vasculitis

DX

GROIN Candidal intertrigo Erythrasma Hailey-Hailey disease Hidradenitis suppurativa Psoriasis Seborrheic dermatitis Seborrheic keratosis Skin tag Tinea cruris

GENITALIA Herpes simplex Lichen planus Lichen sclerosus Molluscum contagiosum Psoriasis Scabies Syphilis (chancre) Wart Zoon's balantis

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DX

Dermatoses by Location (Continued) TRUNK

SCALP

Acne Basal cell carcinoma Cherry angioma Darier disease Drug eruption Epidermal cyst Folliculitis Grover disease Keloid Lipoma Melanoma Molluscum contagiosum Morphea Mycosis fungoides Neurofibroma Nevus Pityriasis rosea Psoriasis Seborrheic keratosis Skin tag Striae Syphilis Tinea corporis Tinea versicolor Urticaria Varicella-zoster infection

Actinic keratosis Alopecia areata Androgenetic alopecia Dermatitis Epidermal or pilar cyst Nevus Pediculosis (lice) Psoriasis Seborrheic dermatitis Squamous cell carcinoma Tinea capitis

AXILLA Acanthosis nigricans Allergic contact dermatitis Erythrasma Hailey-Hailey disease Hidradenitis suppurativa Hyperhydrosis Seborrheic dermatitis Skin tag Tinea corporis

HANDS Actinic keratosis Atopic eczema Contact dermatitis Erythema multiforme Granuloma annulare HFMD Hyperhidrosis Keratoacanthoma Lichen planus Psoriasis Scabies Syphilis Warts

FEET Contact dermatitis Corn Granuloma annulare HFMD Keratoderma Lichen planus Nevus Onychomycosis Plantar wart Psoriasis Tinea pedis

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17 Dermatoses by Location (Continued) Racial pigmentation (gums and buccal mucosae) Candidiasis Vesicle of HFMD Angular cheilitis (corner of mouth)

Lichen planus

Leukoplakia Aphthous ulcer Migratory glossitis

Fissured tongue

Diagnostic Hints: What to Do When You’re Uncertain Did you consider: 1. Drug eruption? 2. Factitial? 3. Lupus erythematosus? 4. Mycosis fungoides? 5. Occupational or hobbies? 6. Sarcoidosis?

DX

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DX 7. Scabies? 8. Syphilis? 9. Systemic illness? Did you think of these broad categories? 1. Infectious: E.g., bacterial, fungal, parasitic, spirochetal, viral 2. Neoplastic 3. Inflammatory/autoimmune 4. Allergic: E.g., contact dermatitis 5. Drug reaction 6. Metabolic 7. Genetic Did you examine for or enquire about: 1. Focus of infection? 2. Foreign travel? 3. Mucosal clues? 4. Nail clues? 5. Over-the-counter, herbal, or natural medicines? 6. Pets? 7. Scalp clues? 8. Tinea pedis? 9. Tumor? Did you: 1. Biopsy? 2. Culture? 3. Envision the lesion at another site? 4. Order blood studies? 5. Order imaging studies? 6. Patch test? 7. Perform a KOH? 8. Really listen to the patient?

Diagnostic Hints Courtesy of Dr. Walter B. Shelley.

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19 Pruritus/Itch Causes of Localized Pruritus Body Region Scalp Trunk

Groin Anal region Hands Legs

Feet

Examples Pediculosis capitis (lice), psoriasis, seborrheic dermatitis Contact dermatitis (axillae, waistline), erythrasma (axillae), pediculosis corporis, psoriasis, scabies, seborrheic dermatitis (chest), seborrheic keratoses, urticaria Candida, contact dermatitis, erythrasma, pediculosis pubis, scabies, tinea cruris Candidiasis, contact dermatitis, gonorrhea, hemorrhoids, pinworms, psoriasis, tinea cruris Contact dermatitis, eczema (atopic, dyshidrotic), scabies Atopic dermatitis, dermatitis herpetiformis (knees), lichen simplex chronicus (malleoli), nummular eczema, stasis dermatitis Contact dermatitis, dyshidrotic eczema, pitted keratolysis, tinea pedis

Causes of Generalized Pruritus Body Region Skin diseases

Endocrine disorders

Examples Contact dermatitis; dermatitis herpetiformis; eczema—atopic, nummular, bullous pemphigoid, mycosis fungoides, psoriasis, PUPPP, urticaria, xerosis Carcinoid syndrome, diabetes, hypo- & hyperthyroidism (Continued text on following page)

DX

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DX

Causes of Generalized Pruritus (Continued) Body Region

Examples

Infectious diseases Hepatitis C, HIV, pediculosis, scabies Psychiatric disease Anxiety, delusions of parasitosis, depression Systemic Chronic renal failure, drugs (medicine, drugs of disease addiction/abuse), hemochromatosis, hepatic cholestasis, pregnancy (e.g., cholestasis of pregnancy), primary biliary cirrhosis Hematopoietic Hodgkin’s disease, iron deficiency, anemia, disorders lymphoma, polycythemia rubra vera

Skin Manifestations of Systemic Disease Skin Manifestations of Chronic Renal Failure Changes in skin pigmentation: Bruising, hyperpigmented palms & soles, pallor, photodistributed or diffuse hyperpigmentation, uremic frost, yellow tinge Infections: Onychomycosis, tinea pedis Nail changes: Half-and-half nails, pale nails, splinter hemorrhages Pruritus Xerosis Keratotic palmoplantar pits Perforating disorders: Kyrle disease, reactive perforating collagenosis Calcinosis cutis

Skin Manifestations of Endocrine Diseases Acromegaly: Acanthosis nigricans, soft tissue hypertrophy, seborrheic dermatitis Addison’s disease: Increased skin pigmentation Cushing’s syndrome: Acanthosis nigricans, acne, fat maldistribution (e.g., “Buffalo hump”), hirsutism, ruddy skin with telangiectasia, striae, thin & atrophic skin

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21 Diabetes: Acanthosis nigricans, bullous diabeticorum, diabetic dermopathy, foot ulcers, fungal & bacterial skin infections, granuloma annulare (controversial), necrobiosis lipoidica (diabeticorum), pruritus, scleredema, skin tags, yellow skin & nails Hyperthyroidism: Fine hair, hair loss, hyperhidrosis, onycholysis, pretibial myxedema, pruritus, warm smooth skin Hypothyroidism: brittle nails, broken hair, coarse hair, diffuse hair loss, loss of outer third of eyebrow, pruritus, thickened yellow skin, xeroderma

Skin Manifestations of Gastrointestinal Diseases Acrodermatitis enteropathica: Abnormality in zinc absorption Dermatitis herpetiformis: Gluten-sensitive enteropathy Eczema (flexural): Malabsorption, mild zinc deficiency Gardner’s syndrome: Large intestinal polyps Liver disease, chronic: Dilated abdominal wall veins, gynecomastia, jaundice, loss of body hair, palmar erythema, peripheral edema, purpura, spider angiomas, Perineal ulceration, sinus tracts: Crohn’s disease Peutz-Jeghers syndrome: Small intestine polyps Pyoderma gangrenosum: Crohn’s disease, rheumatoid arthritis, ulcerative colitis

Skin Manifestations of Other Systemic Diseases Hyperlipidemia: Xanthomas—tendinous, tuberous, eruptive Neurofibromatosis: Café au lait macules, freckling (axillary, inguinal; “Crowe’s sign”), multiple cutaneous neurofibromas Pellagra (nicotinic acid deficiency): 3Ds—dementia, dermatitis, diarrhea; erythema following sun exposure Porphyria: Blister formation, hypertrichosis, milia, photosensitivity, pigmentation, skin fragility Sarcoidosis: Blue-red subcutaneous nodules, lupus pernio, sarcoid in scar Scurvy: Bleeding gums, coiled hairs, perifollicular purpura, poor wound healing Tuberous sclerosis: Confetti macules, enamel pits, facial angiofibromas, forehead plaque, gingival fibromas, hypomelanotic macules, periungual fibromas, Shagreen patch

DX

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DX

Nails Nail bed Cuticle Nail plate

Eponychium Nail matrix

Distal nail fold

Posterior ligament

Anterior ligament Distal edge of nail plate

Nail plate

Cuticle

Lateral nail fold Lunula

Eponychium

Onycholysis

Longitudinal band Pitting

Beau's lines Mee's or Meuhrcke's lines

22

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23 Nail Findings and Associated Systemic Conditions Nail Finding

Associated Systemic Condition

Shape or Growth Change Beau’s lines

Clubbing

Koilonychia

Onycholysis

Pitting Yellow nail

Any severe systemic illness that disrupts nail growth, pemphigus, Raynaud’s disease, trauma Asbestosis, atrioventricular malformations, chronic bronchitis, cirrhosis, congenital heart disease, COPD, endocarditis, fistulas, inflammatory bowel disease, pulmonary malignancy Hemochromatosis, iron deficiency anemia, nail-patella syndrome, Raynaud’s disease, SLE, trauma Amyloidosis, connective tissue disorders, hyperthyroidism, infection, psoriasis, sarcoidosis, trauma Alopecia areata, incontinentia pigmenti, psoriasis, Reiter’s syndrome Bronchiectasis, immunodeficiency, lymphedema, nephrotic syndrome, pleural effusion, Raynaud’s disease, rheumatoid arthritis, sinusitis, thyroiditis, tuberculosis

Color Change Azure lunula Dark longitudinal streaks Half-and-half nails Longitudinal striations

Hepatolenticular degeneration (Wilson’s disease), quinacrine therapy, silver poisoning Benign nevus, chemical staining, melanoma, normal variant in darkly pigmented people Specific for renal failure Alopecia areata, atopic dermatitis, vitiligo, psoriasis (Continued text on following page)

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Nail Findings and Associated Systemic Conditions (Continued) Nail Finding

Associated Systemic Condition

Mees’ lines

Muehrcke’s lines Splinter hemorrhage

Telangiectasia Terry’s (white) nails

Arsenic poisoning, carbon monoxide poisoning, chemotherapy, CHF, Hodgkin’s disease, leprosy, malaria, other systemic insults Specific for hypoalbuminemia Antiphospholipid syndrome, malignancies, oral contraceptive use, pregnancy, psoriasis, rheumatoid arthritis, SLE, subacute bacterial endocarditis, trauma Dermatomyositis, rheumatoid arthritis, scleroderma, SLE Cirrhosis, CHF, diabetes mellitus, hepatic failure, hyperthyroidism, malnutrition

Skin Disorders With Nail Changes Disease

Incidence

Alopecia areata Darier’s disease

10% High

Eczema

Common

Lichen planus

10%

Pityriasis rubra pilaris Psoriasis

Majority

Scleroderma

Frequent

Findings Fine pits, rough nail surface Longitudinal ridging, red & white longitudinal bands, V-neck, hyperkeratosis Coarse pitting, shiny nails, transverse ridging Coarse pitting, shiny nails, transverse ridging Hyperkeratotic, yellow-brown

10%–50%

“Oil spots,” onycholysis, pits, splinter hemorrhages, subungual hyperkeratosis Pterygium inversus unguium

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25 Drug Eruptions in Dermatology Typical presentations (in descending order of frequency): Exanthema (maculopapular, morbilliform) Urticaria and angioedema Fixed drug eruptions Erythema multiforme Stevens-Johnson syndrome Exfoliative dermatitis Photosensitivity reactions Anaphylaxis Toxic epidermal necrolysis Drugs most commonly resulting in an adverse skin reaction: Amoxicillin Trimethoprim-sulfamethoxazole Ampicillin Whole blood Cephalosporins Allopurinol Carbamazepine

Drugs Causing Skin Pigmentation Changes Color

Drug Gold ACTH, bleomycin, minocycline, oral contraceptives, zidovudine Amiodarone, antimalarials, minocycline, phenothiazines Clofazimine Beta-carotene, quinacrine

Blue-gray Brown Gray Red Yellow

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Drug Eruptions & Likely Patterns Drug Antimalarials Barbiturates Beta-blockers Iodides and bromides Minocycline Penicillamine Penicillins, sulfonamides Phenothiazines Salicylates

Pattern of Eruption Lichen planus–like eruption Blistering of lower limbs Psoriasiform Acneiform eruption Hyperpigmentation Pemphigus-like eruption Morbilliform, erythema multiforme, SLE Photosensitive dermatosis Angioedema, urticaria

Skin Reaction Patterns & Drugs That Cause Them Reaction Pattern Acne Alopecia Erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis Erythema nodosum Erythroderma Exfoliative dermatitis Photosensitivity Psoriasiform eruptions SLE-like syndrome

Likely Drugs Corticosteroids, lithium Anti-thyroid drugs, coumarin anticoagulants, cytotoxics (e.g., chemo) Allopurinol, antibiotics, anticonvulsants, NSAIDs, sulfonamides

Oral contraceptives, sulfonamides Antibiotics, anti-rheumatic drugs Gold, isoniazid, phenylbutazone Phenothiazines, tetracyclines Antimalarials, beta-blockers, lithium Hydralazine, minocycline, penicillin, sulfonamides (Continued text on following page)

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27 Skin Reaction Patterns & Drugs That Cause Them (Cont’d) Reaction Pattern Toxic erythema

Vasculitic and purpuric eruptions

Likely Drugs Antibiotics (e.g., ampillicin), antirheumatics, barbiturates, sulfonamides Indomethacin, phenytoin

Effects of Aging on Skin Intrinsic HISTOPATHOLOGIC Decreased: corneocyte adhesion, dermal collagen, dermal elastic fibers, dermal ground substance, eccrine sweat glands, epidermal thickness, number of hair follicles, subcutaneous fat (site-dependent) CLINICAL Gray hair, thinning & ridging of nails

Extrinsic (Primarily UV Light) Comedones (e.g., Favre-Racouchot syndrome) Dry skin (xerosis) Elastosis (yellow skin) Freckles Idiopathic guttate hypomelanosis Senile/solar purpura Solar lentigo Telangiectases Venous lakes Wrinkling/rhytides Also: Actinic keratoses, Bowen’s disease, rosacea, roughness, sallow skin tone, seborrheic dermatitis, seborrheic keratoses, skin cancers (BCC, SCC), stasis dermatitis & chronic venous insufficiency, stucco keratoses

Aging Effects by Disease Process Autoimmune: Bullous pemphigoid Benign tumors: Cherry angiomas, chondrodermatitis nodularis helicis, seborrheic keratosis, skin tags

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DX Eczemas: Asteatotic/dry skin, contact, seborrheic Infections: Candidiasis, herpes zoster, onychomycosis, scabies Photodamage: Actinic elastosis, colloid milium, Favre-Racouchot syndrome, freckling, photoaging (wrinkling, solar lentigo), poikiloderma of Civatte Premalignant: Actinic keratosis, Bowen disease Malignancies: BCC, lentigo maligna melanoma, MF, SCC Ulcerations: leg, pressure/decubitus Other: Cutaneous horn, pruritus

Effects of Pregnancy on Skin Dermatoses of Pregnancy 1. Pemphigoid gestationis/herpes gestationis 2. Cholestasis of pregnancy 3. Pruritic urticarial papules and plaques of pregnancy (PUPPP)/polymorphic eruption of pregnancy (PEP) 4. Prurigo of pregnancy—may include pruritic folliculitis #1,2: Fetal risks; #3,4: no fetal risks.

Pigmentary Changes of Pregnancy 1. Hyperpigmentation: anogenital region, areola-nipple complex, axillae, inner thighs 2. Linea nigra on abdomen 3. Melasma 4. Nevi and freckles darken

Vascular Changes of Pregnancy 1. 2. 3. 4. 5. 6. 7. 8.

Gingival hyperemia or hyperplasia Hemorrhoids Nonpitting edema Palmar erythema Pyogenic granulomas Spider angiomas Varicose veins Vasomotor instability

Note: Impetigo herpetiformis (acute form of pustular psoriasis in pregnancy) no longer considered a specific dermatosis of pregnancy.

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29 Hair Changes of Pregnancy 1. Hirsutism 2. Postpartum telogen effluvium 3. Postpartum androgenetic alopecia

Nail Changes of Pregnancy (None are Pathognomonic) 1. 2. 3. 4.

Subungual hyperkeratosis Onycholysis Transverse grooving Brittleness

Connective Tissue Changes of Pregnancy Striae gravidarum/stretch marks (in up to 90%)

Glandular Changes of Pregnancy 1. Increased eccrine & sebaceous function 2. Decreased apocrine function

Diseases Potentially Improved During Pregnancy 1. 2. 3. 4. 5. 6. 7.

Acne Atopic dermatitis Fox-Fordyce disease Hidradenitis suppurativa Psoriasis Rheumatoid arthritis Sarcoidosis

Diseases Potentially Worsened During Pregnancy 1. Infections: Candida vaginitis, condyloma acuminata, herpes simplex, leprosy, pityrosporum folliculitis, trichomoniasis, VZV 2. Immune-mediated diseases: Dermatomyositis/polymyositis, lupus erythematosus, pemphigus vulgaris, systemic sclerosis 3. Metabolic diseases: Acrodermatitis enteropathica, porphyria cutanea tarda 4. Connective tissue disorders: Ehlers-Danlos syndrome, pseudoxanthoma elasticum 5. Miscellaneous: AIDS, cutaneous T-cell lymphoma, erythrokeratoderma variabilis, hereditary hemorrhagic telangiectasia, neurofibromatosis

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Dermatologic Emergencies Vesiculobullous Disorders Stevens-Johnson syndrome, toxic epidermal necrolysis, pemphigus vulgaris, other generalized blistering disorders (e.g., bullous pemphigoid)

Infections Cysticercosis cutis, hemorrhagic fevers, leprosy (reversal reaction upon treatment) mucormycosis, necrotizing fasciitis & other gangrene (e.g., gas gangrene, progressive bacterial synergistic gangrene), neonatal herpes simplex, Rocky Mountain spotted fever, Still’s disease, trichinosis, tularaemia

Autoimmune Disorders Acute eruption, systemic and neonatal lupus erythematosus & dermatomyositis

Inflammatory Cutaneous Disorders Acne fulminans, acute drug eruptions (e.g., red man syndrome), acute pustular psoriasis, capillary hemangiomas (affecting respiratory tract or oral cavity, periorbital), exfoliative erythroderma, Kawasaki syndrome, pyoderma gangrenosum, scarring alopecias (“hair emergency”)

Environmental Burns, child abuse, cholesterol emboli, sclerema neonatorum

Presentation and Worrisome Differential 1. Generalized red rash with fever a. Bacterial infections with toxin production b. Drug eruptions c. Rickettsial exanthems d. Viral exanthems 2. Generalized red rash with blisters and prominent mouth lesions a. Bullous pemphigoid b. Drug eruptions c. Erythema multiforme (major) d. Toxic epidermal necrolysis

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31 3. Generalized rash without redness with blisters, erosions, and mouth lesions a. Pemphigus 4. Generalized red rash with pustules a. Drug eruptions b. Pustular psoriasis 5. Generalized rash with vesicles a. Disseminated herpes simplex b. Drug eruptions c. Generalized herpes zoster d. Varicella 6. Generalized red rash with scaling over whole body a. Exfoliative erythroderma 7. Generalized wheals and soft tissue swelling a. Urticaria and angioedema 8. Generalized purpura a. Drug eruptions b. Purpura fulminans c. Thrombocytopenia 9. Generalized purpura that can be palpated a. Bacterial endocarditis b. Vasculitis 10. Multiple skin infarcts a. Disseminated intravascular coagulopathy b. Gonococcemia c. Meningococcemia 11. Localized skin infarcts a. Antiphospholipid antibody syndrome b. Atheroembolization c. Atherosclerosis obliterans d. Calciphylaxis e. Warfarin necrosis 12. Facial inflammatory edema with fever a. Erysipelas b. Lupus erythematosus Reprinted with permission from Fitzpatrick’s Color Atlas and Synopsis of Clinical Dermatology, edition 5 by Wolff, Suurmond, and Johnson. McGraw-Hill Professional Publishing.

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Topical Medication Vehicles Ointment

■ Emulsion of water in oil ■ Greasy vehicle that provides enhanced penetration; occlusive, therefore don’t use on infected or oozing skin ■ #1 (most lubricating) for dry skin, hyperkeratotic, and lichenified lesions (e.g., psoriasis, lichen simplex chronicus, chronic eczema)

Cream

■ Emulsion of oil in water ■ Less moisturizing than ointments, but more cosmetically appealing ■ Useful in acute and subacute dermatoses

Gel ■ ■ ■ ■

Usually alcohol-based, transparent and colorless Liquefies on contact with skin Nongreasy, non-occlusive, nonstaining Use in hair-bearing areas or when drying is desired

Solution

■ A liquid vehicle: propylene glycol, water or alcohol ■ Useful under cosmetics, in hair-bearing regions, and when drying is desired

Lotion

■ Suspension of a powder in water; leaves a film of uniform powder on skin ■ Less moisturizing than a cream ■ Good for hair-bearing areas

Foams

■ Any area, but especially scalp ■ Easy application, with less grease/residue

Powders

■ Promote drying ■ Used in intertriginous areas to reduce moisture, friction, maceration

Paste

■ Mixture of powder and ointment ■ Ihle’s paste used for diaper and intertriginous dermatitis

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33 Topical Steroids Memorize and become comfortable prescribing 1 to 2 topical steroids within each steroid potency group.

Potency*

1 (Most Potent) Cormax—Clobetasol propionate Diprolene—Betamethasone dipropionate Olux—Clobetasol propionate Psorcon—Diflorasone diacetate Temovate—Clobetasol propionate Ultravate—Halobetasol propionate

0.05% (cream, ointment, solution) 0.05% (optimized vehicle; ointment) 0.05% (foam) 0.05% (optimized vehicle; ointment) 0.05% (optimized vehicle; cream, ointment) 0.05% (cream, ointment)

2 Cyclocort—Amcinonide Diprolene AF—Betamethasone dipropionate Diprosone—Betamethasone dipropionate Elocon—Mometasone furoate Florone—Diflorasone diacetate Halog—Halcinonide Kenalog—Triamcinolone acetonide Lidex—Fluocinonide Maxiflor—Diflorasone diacetate Topicort—Desoximetasone

0.1% (ointment) 0.05% (cream) 0.05% (ointment) 0.1% (ointment) 0.05% (ointment) 0.1% (cream) 0.5% (ointment) 0.05% (cream, gel, ointment) 0.05% (ointment) 0.25% (cream, ointment), 0.05% (gel)

3 Aristocort A—Triamcinolone acetate Aristocort HP—Triamcinolone acetate Benisone—Betamethasone benzoate Cutivate—Fluticasone propionate

0.1% (ointment) 0.5% (cream) 0.025% (gel) 0.005% (ointment)

*N.B.: Occlusion (e.g., under saran wrap) can increase potency 10 to 100 times.

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TX Cyclocort—Amcinonide Diprosone—Betamethasone dipropionate Florone—Diflorasone diacetate Halog—Halcinonide Lidex E cream—Fluocinonide Luxiq—Betamethasone valerate Maxiflor—Diflorasone diacetate Topicort LP emollient cream—Betamethasone Uticort—Betamethasone benzoate Valisone—Betamethasone valerate

0.1% (cream, lotion) 0.05% (cream) 0.05% (cream) 0.1% (ointment) 0.05% (cream) 1.2 mg/g (foam) 0.05% (cream) 0.05% (cream) 0.025% (gel) 0.1% (ointment)

4 Aristocort—Triamcinolone acetonide Benisone—Betamethasone benzoate Cordran—Flurandrenolide Elocon—Mometasone furoate Halog—Halcinonide Kenalog—Triamcinolone acetonide Synalar HP—Fluocinolone acetonide Synalar—Fluocinolone acetonide Topicort LP—Desoximetasone Uticort—Betamethasone benzoate Valisone—Betamethasone valerate Westcort—Hydrocortisone valerate

0.1% (ointment) 0.025% (ointment) 0.05% (ointment) 0.1% (cream) 0.025% (cream) 0.1% (ointment) 0.2% (cream) 0.025% (ointment) 0.05% (cream) 0.025% (ointment) 0.1% (lotion) 0.2% (ointment)

5 Aristocort—Triamcinolone acetonide Benisone—Betamethasone benzoate Betatrex—Betamethasone valerate Cloderm—Clocortalone Cordran—Flurandrenolide Cutivate—Fluticasone propionate Dermasmoothe/FS—Fluocinolone acetonide Dermatop—Prednicarbate Diprosone—Betamethasone dipropionate Fluonid—Fluocinolone acetonide Locoid—Hydrocortisone butyrate Synalar—Fluocinolone acetonide Uticort—Betamethasone benzoate Valisone—Betamethasone valerate Westcort—Hydrocortisone valerate

34

0.25% (cream) 0.025% (cream) 0.1% (cream) 0.1% (cream) 0.05% (cream) 0.05% (cream) 0.01% (oil) 0.1% (cream) 0.02% (lotion) 0.025% (cream) 0.1% (cream) 0.025% (cream) 0.025% (cream) 0.1% (cream) 0.2% (cream)

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35 6 Aclovate—Aclometasone dipropionate Desowen—Desonide Kenalog—Triamcinolone acetonide Synalar—Fluocinolone acetonide Tridesilon—Desonide Valisone—Betamethasone valerate

0.05% (cream, ointment) 0.05% (cream) 0.1% (cream, lotion) 0.01% (cream, solution) 0.05% (cream) 0.1% (lotion)

7 (Least Potent) Cortaid—Hydrocortisone Decadron phosphate—Dexamethasone Generic—Hydrocortisone Hytone—Hydrocortisone Medrol—Methylprednisolone

0.5%, 1%, 2.5% 0.1% (cream) 0.5%, 1%, 2.5% 0.5%, 1%, 2.5% 1%

General Rules of Use Based on Location Potency Low Intermediate High Ultra-high

Sites Babies’ skin, face, genital skin, skin folds Similar to “Low,” but where skin is more thickened/chronic Scalp; thick or chronic skin lesions Elbows, hyperkeratotic dermatoses, knees, palms, soles

Amounts Required Area Treated

1 Application (g)

Anogenital, face, hands, head 1 arm, posterior or anterior trunk 1 leg Entire body

Bid for 1 Mo (g)

2

28

120

3

42

180

4 30–60

TX

Bid for 1 Wk (g)

56 420–840

240 1.8–3.6 kg

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Use the adult finger-tip unit as your guide Finger-tip measurements 1 finger-tip length = 0.5 g 2 finger-tip lengths = 1 g 1 pump unit = 1g

Topical steroids: approximate single application requirements Adult

Child

1.5 g Face and neck

0.5 g Face and neck

7g Trunk (front and back)

2g Trunk (front and back)

1.5 g One arm

0.5 g One arm

1g One hand

1g Hands and feet

3g One leg

1g One leg

1g One foot

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37 Regional Differences in Penetration: Most to Least 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

Mucous membrane Scrotum Eyelids Face & scalp Chest & back Upper arms & legs Lower arms & legs Dorsa of hands & feet Palmar & plantar skin Nails

Local Skin Side Effects* Acne Atrophy—epidermal, dermal Folliculitis Hirsutism Hypopigmentation Perioral dermatitis Purpura

Rosacea Skin infections—worsened Steroid addiction syndrome Striae Telangiectasia Ulceration Wound healing – delayed

Surgical Procedures Wisdom ■ Elderly patients should slowly sit up and stay seated for a minute following a procedure, as their blood pressure needs time to adjust. ■ Prior to and immediately after surgery, avoid the Gs: gingko, garlic, green tea, ginseng, & ginger (can cause bleeding after surgery). Also avoid Vitamin E and feverfew. ■ Minor bleeding can often be stopped by Monsel’s solution (most effective) or 20% aluminum chloride. ■ To protect yourself medicolegally, ask patients “Do you not like the cosmetic appearance of this?” before cosmetic removal of SKs, moles, etc.

*N.B.: These are uncommon if the correct potency is used in the correct location, for the appropriate duration.

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TX ■ To protect yourself from needle sticks, make a rule in your office that whomever uses a sharp object, disposes of that object. Never recap a needle. ■ For small lesions, hand patients a mirror to point them out. You don’t want to treat the wrong lesion. ■ If using liquid nitrogen cryotherapy for warts/molluscum in kids, apply Maxilene 5 (or EMLA) by swab immediately after treatment to reduce pain. ■ Dark-skinned patients and those having procedures on the upper back, shoulders or chest should always be warned of the risk of keloids. ■ Consider having consent forms for every surgical, and certainly any cosmetic procedure.

Pregnancy Categories of Medication FDA Pregnancy Drug Risk Categories Drug Risk Category X

D

C

B

A Unrated

Definition Contraindicated in pregnancy No reason to risk use of drug in pregnancy. Evidence for risk to human fetus However, benefits may outweigh risks of drug. Risk cannot be ruled out—human studies lacking. Animal studies may or may not show risk. Potential benefits may justify potential risk. No risk to human fetus despite possible animal risk. Or no risk in animal studies, and human studies have not been performed. Controlled studies show no fetal risk. No pregnancy category assigned.

38

A

C

X

Fluorouracil Tazarotene Acitretin Bexarotene Estrogens Finasteride Isotretinoin Leflunomide Methotrexate Thalidomide


Mechlorethamine Nitrogen mustard Aldactone/ Spironolactone Azathioprine Bleomycin Carmustine Colchicine Cyclophosphamide Danazole Flutamide Hydroxyurea Kanamycin Potassium iodide Progestogens Streptomycin Tetracyclines

D

Dermatologic Drugs in Pregnancy

B

Adapalene Anthralin Bacitracin Benzoyl peroxide Calcipotriene Coal tar Crotamiton Hydroquinone Ketoconazole Levulan Kerastick Minoxidil Pimecrolimus Podophyllum Sodium sulfacetamide Steroids Sulfur Tacrolimus

Topical drugs are in blue.

U Cantharidine Nystatin Resorcin Salicylic acid* Ivermectin Azelaic acid Bactroban Ciclopirox Clindamycin Clotrimazole EMLA Erythromycin Imiquimod Lindane Malathion Metronidazole Mupirocin Naftifine Penlac Permethrin Silver sulfa* Terbinafine Zonalon Acetaminophen

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39

U

B

C

X


D

Dermatologic Drugs in Pregnancy (Continued) A

Alefacept Tretinoin Azithromycin Vaniqa Cephalosporins Acyclovir Cetirizine Aspirin ChlorpheniBactrim/Septra ramine Beta carotene Cimetidine Chloroquine CyproheptaCiprofloxacin dine Clotrimazole DiphenhydCodeine ramine Cyclosporine Etanercept Dapsone Erythromycin Denileukin Famciclovir Difitox Ibuprofen Efalizumab Infliximab Fexofenadine Loratadine Fluconazole Metronidazole Fluoroquinalones Nystatin Gold Griseofulvin

40


TX

U

B

C

D

Dermatologic Drugs in Pregnancy (Continued) A Penicillins Prednisone Sulfasalazine Tacrolimus Terbinafine Valacyclovir

Hydroxychloroquine Infliximab Interferons Itraconazole Ivermectin IVIG Kenalog— intralesional Ketoconazole Methoxsalen Mycophenolate mofetil Nicotinomide Psoralens Rifampin Steroids Sulfonamides Thiabendazole Trimethoprim *Should be avoided in late pregnancy.

X

TX


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Cryotherapy

Liquid nitrogen—direct from spray canister (⫺195.8 ⬚C) or a dipped swab (much less cold) Liquid nitrogen cryotherapy is most commonly used for: actinic keratoses, Bowen disease (SCC in-situ), molluscum contagiosum, myxoid cysts, pyogenic granulomas, skin tags, solar lentigines, and warts. (See Image B on page 43.)

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43 Punch Biopsy A

1

2

3

4

B

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X-rays

UVB: 290–320nm UVC: 100–290nm

Photobiology & Phototherapy

Vacuum UV

200

UVC

Atmospheric ozone

x-rays

Ultraviolet

320

Visible

Visible

400

400

UVA

Sunscreens

UVB

UVA1 340 400 Wavelength (nm)

UVA2

Skin cancer/aging

Pigmentation

Sunburn

290

Window glass

200

Infrared

Infrared

Electromagnetic Spectrum with Expanded UV Region

UVA: 320–400nm (UVA-1 ⫽ 340–400nm; UVA-2 ⫽ 320–340nm)

Gamma rays (nm) Blockers of UV γ-rays (nm) Skin changes and the responsible wavelengths

(nm) 320

Radio waves

44


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45 Penetration of Different UV Wavelengths UVC 200 – 290 nm

UVB 290 – 320 nm

UVA 320 – 400 nm

Stratum corneum Epidermis

Dermis

Subcutaneous fat Human Skin Phototypes (SPT) Skin Unexposed Phototype Skin Color I II III

White White White

IV V VI

Light brown Brown Dark brown

Sun Response History Always burns, never tans Always burns, minimally tans Burns minimally, tans gradually and uniformly Burns minimally, always tans well Rarely burns, tans darkly Never burns, tans darkly

*Those in SPT groups I & II are at highest risk for skin cancer.

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Photocarcinogenic Cascade UV exposure

DNA damage

Formation of mutations

Malignant transformation

Phototherapy is particularly helpful for: ■ Eczema/atopic dermatitis ■ Mycosis fungoides/cutaneous T-cell lymphoma ■ Palmoplantar pustulosis ■ Parapsoriasis ■ Pityriasis rosea ■ Polymorphous light eruption (prevention) ■ Pruritus (esp. in renal failure) ■ Psoriasis ■ Vitiligo

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47 ■ Other diseases may be helped: acne, alopecia areata, graftversus-host disease, granuloma annulare, Langerhans cell histiocytosis, lichen planus, localized scleroderma, lymphomatoid papulosis, photodermatoses, pityriasis lichenoides, and urticaria pigmentosa Photo/sun-aggravated dermatoses: ■ Acne vulgaris (small %; most improve) ■ Atopic dermatitis (small %; most improve) ■ Bullous pemphigoid ■ Darier disease ■ Dermatomyositis ■ Disseminated superficial actinic porokeratosis ■ Erythema multiforme ■ Grover disease ■ Hailey-Hailey disease ■ Lichen planus ■ Lupus erythematosus ■ Mycosis fungoides/cutaneous T-cell lymphoma (small %; most improve) ■ Pellagra ■ Pemphigus ■ Pityriasis rubra pilaris ■ Porphyria ■ Psoriasis (small %; most improve) ■ Rosacea ■ Seborrheic dermatitis ■ Viral infections—e.g., HSV Drugs causing photosensitivity: ■ ACE inhibitors ■ Amiodarone ■ Ciprofloxacin ■ Nifedipine ■ NSAIDs ■ Phenothiazines ■ Sulfonamides ■ Tetracyclines (esp. doxycycline) ■ Thiazides

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Lasers Laser Wavelengths Laser

Wavelength

Target

Uses

Resurfacing Lasers Carbon dioxide 10,600 nm (CO2) laser 2940 nm Erbium:YAG laser

Water

Resurfacing

Water

Resurfacing; more superficial

488, 514 nm

Oxyhemoglobin

Argon-pumped 585–690 nm tunable dye

Oxyhemoglobin

Telangiectases, thick port-wine stains, venous lesions; high risk of scarring Telangiectases, thick port-wine stains Telangiectases, thick port-wine stains Telangiectases, thin port-wine stains, cherry angiomas, childhood hemangiomas, warts, scars, striae, poikiloderma of Civatte, leg veins

Vascular Lesion Lasers Argon*

Copper vapor, yellow*

578 nm

Oxyhemoglobin

Flashlamp pulsed dye

585, 595 nm

Oxyhemoglobin


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49 Laser Wavelengths (Continued) Laser Krypton, yellow*

Wavelength

Target

Uses

1568 nm

Oxyhemoglobin

Long-pulsed 532 nm KTP Long-pulsed 1064 nm Nd: YAG (safest in dark skin types)

Oxyhemoglobin Oxyhemoglobin

Telangiectases, thin port-wine stains Facial telangiectases, leg veins Leg veins

Pigmented Lesion Lasers Copper vapor, green* Frequencydoubled Nd: YAG

511 nm

Melanin

532 nm

Melanin

Krypton, green*

521, 531 nm

Melanin

755 nm 810 nm 1064 nm 694 nm

Melanin Melanin Melanin Melanin

Epidermal pigmented lesions Epidermal pigmented lesions, some red tattoos Epidermal pigmented lesions

Hair Removal Lasers** Alexandrite Diode Nd:YAG Ruby

in in in in

hair hair hair hair

Hair Hair Hair Hair

removal removal removal removal


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Laser Wavelengths (Continued) Laser

Wavelength

Target

Uses

Tattoo Lasers Frequencydoubled Nd: YAG Q-switched alexandrite Q-switched Nd: YAG Q-switched ruby

532 nm

Tattoo pigment Red tattoos

755 nm

Tattoo pigment Black, blue, and green tattoos Tattoo pigment Black and blue tattoos Tattoo pigment Black, blue, and green tattoos; Nevus of Ota

1064 nm 694 nm

*These lasers are uncommonly used **Only effective on darkly pigmented hair; blond or gray hair resists treatment N.B. #1: Q-switched technology allows higher energy & shorter pulses. N.B. #2: New laser technology: 1. Excimer laser (308 nm): psoriasis, striae & vitiligo 2. 1450 diode or 1320 Nd:YAG laser: dermal collagen remodeling for wrinkles and atrophic scars.

50

Stratum corneum Epidermis

Dermis

Dermal vessels Subcutaneous fat

KTP 532 nm

PDL Ruby Alexandrite Diode Nd:YAG 585-600 694 755 800 1064 nm nm nm nm nm

Depth of Penetration by Various Lasers Excimer Nd:YAG CO2 Argon 193 2940 10,600 488-514 nm nm nm nm

TX


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A-F

Acanthosis Nigricans (AN)

Etiology: May be due to: a. Heredity b. Endocrine disorder—most commonly associated with insulin resistance (i.e., diabetes mellitus), hyperandrogenic state, hypothyroidism c. Obesity d. Drugs—e.g., nicotinic acid, niacinamide, oral contraceptives, steroids e. Malignancy, usually adenocarcinoma—e.g., gastrointestinal (60% stomach), lung, breast History: Rule out aforementioned causes. Physical: Hyperpigmented velvety, typically symmetrical plaques predominantly on the neck, axillae, and groin. Physical location & morphology may be similar for AN of different etiologies; hence, Hx and Px should aim to include/exclude these associated conditions. DDx: Eczema (e.g., lichen simplex chronicus), hyperpigmented nevus (e.g., Becker, epidermal), confluent and reticulated papillomatosis of Gougerot and Carteaud Investigations: Screen for diabetes (glycosylated Hgb) and insulin resistance (plasma insulin); consider searching for underlying malignancy in adult onset.

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53 Management ■ Treat underlying disorder (e.g., remove tumor). ■ Cases associated with obesity and/or insulin resistance may improve with weight loss and/or metformin. ■ Management is difficult and mostly for cosmetic purposes. ■ Tx options: Topical tretinoin, ammonium lactate, laser therapy, dermabrasion.

Acne Vulgaris

Inflammatory disorder of pilosebaceous follicles with a 90% prevalence in adolescence and young adulthood.

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A-F Etiology: Abnormal follicular keratinization, increased sebum 2⬚ to androgens, Propionibacterium acnes (bacteria), inflammation. Genetic factors; occlusive cosmetic agents; medications: steroids, ACTH, androgens, danazol, iodides, lithium, antiepileptics, oral contraceptives; diseases: congenital adrenal hyperplasia (CAH), polycystic ovarian syndrome (PCOS); worse with emotional stress. History: Often asymptomatic lesions (especially comedones), although can be tender (nodules). Physical: Two types of lesions, predominantly affect face, neck, chest and back. a. Noninflammatory—open (“black heads”) and closed (“white heads”) comedones. b. Inflammatory—papules, pustules, cysts, nodules; deep lesions leave scars, inflammatory papules, pustules & nodules on back and check with early scarring. DDx: Folliculitis, perioral dermatitis, rosacea Investigations: If irregular periods, hirsutism, virilization, or not responding to conventional therapy, work-up to rule out virilizing tumor or PCOS.

Management Treatment Options Based on Acne Type Treatment

Comedonal

Inflammatory Nodulocystic

Topical Therapy Salicylic acid Retinoids Azelaic acid Benzoyl peroxide Antibiotics

X X X X X

X X X X

Systemic Therapy Oral contraceptives Antibiotics Isotretinoin

X

X X X

X

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55 Selected Topical Medications for the Treatment of Acne Medication

Dosage

Side Effects

Retinoids* Adapalene (Differin) Tazarotene (Tazorac) Tretinoin (Retin-A)

Qhs–bid

Tretinoin microsphere (Retin-A Micro)

Qhs

Qhs Qhs

Same as tretinoin but less severe Same as tretinoin but more severe Dryness, scaling, erythema, burning, irritation, and photosensitivity Same as tretinoin but less severe

Antibiotics Clindamycin Erythromycin

Qd–bid Qd–bid

Local irritation, dryness Local irritation, dryness

Azelaic acid (Azelex)

Qd–bid

Benzoyl peroxide (2.5%–10%)

Qd–bid

Salicylic acid (StriDex, Clearasil) Sulfacetamide (Klaron) Sulfacetamide/ sulfur (Sulfacet-R) Combination products (Duac, Benzamycin)

Qd–bid

Dryness, scaling, erythema, burning, irritation, pruritus; rarely, hypopigmentation Erythema, peeling, contact dermatitis, dryness, bleaches bedding/clothing Dryness, irritation

Other

Itching, redness, irritation; contraindicated if sulfa allergy Same as sulfacetamide

Bid Bid Qd–bid

Erythema, peeling, contact dermatitis, dryness, bleaches bedding/clothing

*Due to irritation, retinoids can be used every second day or as tolerated.

A-F

Medication

Same as doxycycline (except less photosensitivity), plus rare lupus-like syndrome, or rare hypersensitivity reaction, and skin and mucous membrane hyperpigmentation Common: cheilitis, dry skin and mucous membranes, pruritus, epistaxis, conjunctivitis, photosensitivity, arthralgia, hypertriglyceridemia, elevated liver transaminase levels, decreased night vision Rare: pseudotumor cerebri, hepatotoxicity, major birth defects (Counsel regarding birth control/abstinence), cataracts, neutropenia, thrombocytopenia, reported cases of depression

N/V/D, abdominal pain and cramps, rash, stomatitis, elevated liver transaminase levels, jaundice N/V/D, photosensitivity, stomatitis, discolored teeth (if ⬍8 yr), esophagitis, lightheadedness, dizziness, vertigo, headache, pseudotumor cerebri Same as doxycycline

Side Effects

Selected Systemic Medications Acne Treatment Dosage

Erythromycin 250 mg bid–qid; with meals Doxycycline 50–100 mg qd–bid (or 20 mg bid subantimicrobial dose); with meals Tetracycline 500 mg bid; take on empty stomach 50–100 mg qd–bid; with meals Minocycline

Isotretinoin

Start at 0.5–1 mg/kg/day. After 1 mo, full dose of 1 mg/kg/day to cumulative dose of 120–150 mg/kg (usually 15–20 wk) Lab tests: CBC, TG, ALT, B-hCG— baseline & monthly N/V/D⫽5-nausea/vomiting/diarrhea.

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57 ■ Other options: comedone extraction, intralesional cortisone injection (for papulonodules, cysts), oral contraceptives (esp. anti-androgenic such as cyproterone acetate, Yasmin®), photodynamic therapy, spironolactone (reduces androgen production; 50–200 mg/day); dermabrasion, chemical peels ■ Treatment improves cosmesis and psychosocial well-being, and helps prevent further scarring and hyperpigmentation. ■ Patients should be forewarned of acne exacerbations in the first month of systemic therapy as deep-seated acne comes to the surface. Also, systemic therapy can require 6 wk before benefits are noted. ■ Isotretinoin should be taken with a fatty snack or meal that has some fat in it

Actinic Keratosis (AK; Solar Keratosis)

Most common precancerous lesions in humans, and more prevalent in fair-skinned individuals who tan poorly and burn easily. Etiology: Sun exposure, ionizing radiation, and arsenic exposure. Physical: Slightly erythematous, rough, scaly papules on sunexposed areas, i.e., head, neck, backs of hands. and forearms. May be difficult to see, but often feel rough: Palpation is essential to diagnosis. Occur on sun-exposed and damaged skin, most commonly in the elderly. Course: ⬍1% of all untreated AKs will progress to squamous cell skin cancer. DDx: BCC, Bowen disease, SCC Investigations: Biopsy if recurrent, unresponsive to treatment, or pronounced hyperkeratosis and induration.

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Management

TX Options

■ Liquid nitrogen cryotherapy for limited # or thick lesions. ■ Electrodessication and curettage, CO2 laser (esp. for actinic cheilitis). ■ Topical 5-fluorouracil (e.g., Efudex®) cream applied bid for 2–4 wk. ■ Imiquimod (Aldara™ 5% cream) applied qd three to five times weekly for 12 wk. ■ Patients must be warned that the treated areas will become irritated, inflamed, and eroded with both 5-fluorouracil and imiquimod; follow-up visit in 1–2 wk to evaluate severity of side effects. ■ Photodynamic therapy, dermabrasion, & chemical peels (for numerous AKs). ■ Multiple lesions are a harbinger of sun damage; patients should be checked annually for AKs and other skin cancers. Biopsy thick lesions or those not responding to above treatment as they may represent invasive squamous cell carcinoma. ■ Sun-awareness and protection advice.

Alopecia

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59 Alopecia (Continued)

Basics of Hair 3 Phases of Hair Development 1. Anagen (growing): 3–7 yr for scalp; 80%–90% of hairs; 50–100 switch to catagen/d (falling out) 2. Catagen (resting): 3–4 wk; 1% of hairs 3. Telogen (shedding): 3 mo; hairs have short club root; 50–100 hairs shed/day; 10%–15% of hairs in this phase N.B.: Normal scalp contains 100,000 hairs. Blonds have 120,000 and those with red hair have 80,000 hairs. There are fewer hairs per square cm in Africans & Asians.

Drug Causes of Hair Loss Drug Class Anticoagulants Antithyroid drugs Cytotoxic drugs

Drug Coumarins, heparin Carbimazole, thiouracil Adriamycin, colchicines, cyclophosphamide, mercaptopurine derivatives, vinca alkaloids

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A-F Diffuse Hair Loss 1. Alopecia areata (diffuse, although most commonly localized) 2. Drug-induced: cytotoxics, anticoagulants, retinoids 3. Endocrine disorders: hypothyroid, hypopituitarism 4. Hair-shaft defects: pili torti, monilethrix 5. Male-pattern baldness/androgenetic alopecia 6. Nutritional: iron deficiency 7. Syphilis 8. Systemic lupus erythematosus 9. Telogen effluvium Localized Hair Loss 1. Alopecia areata 2. Discoid lupus erythematosus 3. Fungal infections (e.g., kerion) 4. Lichen planopilaris 5. Nevoid abnormalities 6. Traction (e.g., corn-rows, ponytails) 7. Trichotillomania

Nonscarring Alopecia: Intact Hair Follicles 1. 2. 3. 4. 5. 6. 7.

Telogen effluvium (TE) Alopecia areata (AA) Anagen effluvium (following chemotherapy) Androgenetic alopecia (AGA): male or female pattern baldness Trichotillomania Infections: fungal (i.e., tinea capitis, kerion) Hair shaft abnormalities

Scarring alopecia: Loss of Hair Follicles 1. Discoid lupus erythematosus (DLE) 2. Lichen planopilaris (LPP) 3. Infections: fungal, bacterial, TB, leprosy N.B.: If scalp biopsy performed (e.g., scarring alopecia), ideally a 4-mm punch biopsy is taken of a symptomatic or early active disease for transverse sectioning and H&E; if lupus suspected, take additional 4-mm punch biopsy—bisect this piece vertically, and submit half for vertical sectioning, and half for DIF. *In general, scarring alopecias should be referred to a dermatologist.

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61 Alopecia Areata

Autoimmune T-cell mediated disease in genetically predisposed persons. Uncommon association with other autoimmune diseases—diabetes, vitiligo, thyroid disease Physical: Well-circumscribed areas of complete hair loss on any hair bearing surface (scalp ⫽ 90%); may see nail pitting; “exclamation point” hairs at periphery of bald patch ■ Totalis ⫽ entire scalp; universalis ⫽ all hair-bearing areas; ophiasis ⫽ hair loss confluent along temporal & occipital scalp DDx: androgenetic alopecia, tinea capitis, trichotillomania, telogen effluvium Investigations: ferritin, TSH, ANA, scalp biopsy if unsure

Management

■ High-potency topical steroids; intralesional triamcinolone acetonide (5–10 mg/cc) q 4–6 wk in adults has best outcome. ■ Some benefit reported with topical anthralin, topical minoxidil. ■ Less commonly: Topical immunotherapy (i.e., diphencyprone), oral steroids (use in early rapidly progressing widespread disease), cyclosporine. ■ Course: 95% regrow in 1 yr (except totalis or universalis, which have poor prognosis); 30% recurrence. ■ Poor prognostic signs: Atopic dermatitis, childhood onset, duration ⬎ 5 yr, onychodystrophy, ophiasis, widespread involvement.

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Androgenetic Alopecia (Male and Female Pattern Baldness)

Etiology: Heredity (polygenic); androgen stimulation Physical: Different pattern for men and women; men—temporal areas affected, progressing to vertex; females—diffuse pattern. DDx: Alopecia areata, anagen/telogen effluvium Investigations: ferritin, TSH, androgen profile (if suspicious of virilization).

Management

■ Topical minoxidil lotion (Rogaine®; 2% or 5%) use daily to stabilize hair loss and regrowth in some cases. ■ Finasteride (Propecia®) 1 mg po qd in men (inhibits synthesis of dihydrotestosterone). ■ Spironolactone 100–200 mg po daily in women. ■ Hair transplantation (from occipital scalp). ■ Hair prosthesis (wig).

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63 Telogen Effluvium

Diffuse decrease in hair density secondary to rapid conversion of anagen to telogen hair. Precipitated by stressful events, illness, fever, pregnancy, crash diet, medications; hair can be shed 2–6 mo after precipitant. Physical: Diffuse hair loss; positive hair pull test (⬎10% club hairs). Investigations: CBC, ferritin, TSH; punch biopsy if unsure. DDx: Alopecia areata, anagen effluvium, androgenetic alopecia.

Management Reassurance. Wait for regrowth, and treat any underlying cause. Topical minoxidil may be beneficial.

Trichotillomania

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A-F Self-induced (neurotic) compulsive hair pulling/plucking. Physical: Circumscribed area of alopecia with irregular borders and broken hairs of different length. May find scalp excoriations and perifollicular petechiae; usually only one area (frontoparietal or frontotemporal) affected. Eyebrows and eyelashes may also be plucked. Investigations: Punch biopsy if unsure. DDx: Alopecia areata, traction alopecia, tinea capitis.

Management

■ When in doubt, biopsy confirms diagnosis. ■ Ask about traumatic events (death, separation, school troubles) ■ Difficult problem; look for precipitant; may need referral to psychiatry (psychotherapy, behavior therapy, SSRIs). ■ Most children outgrow condition, but can be difficult to manage in adults.

Angioma (Cherry Angioma)

Most common benign cutaneous vascular growth, which increases in size and number with age. History: asymptomatic; uncommonly bleeds with trauma

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65 Physical: Cherry-red dome-shaped round papules predominantly on trunk of adults; 0.5–5 mm. Investigations: Biopsy if diagnosis doubtful. DDx: Angiokeratoma, insect bite, melanoma.

Management Treatment for cosmetic purposes Tx options: shave excision, electrodessication, vascular laser, cryotherapy

Angular Cheilitis

Etiology: Mechanical irritation (e.g., intertrigo), infectious (e.g., candidiasis), nutritional (e.g., iron or riboflavin deficiency), contact dermatitis. More common with dentures and in elderly. History: Often chronic; discomfort and burning at corners of mouth.

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A-F Physical: Inflammatory moist fissures radiating down and out from the lip commissures; may observe: atrophy, fissures or maceration, erythema, crusting and scaling of the angles of the mouth. Investigations: Culture to rule out candidiasis & bacterial infection; KOH prep. DDx: Lip-licking dermatitis, impetigo.

Management ■ ■ ■ ■

Improving dentures and/or dentition Topical miconazole or nystatin cream Topical mupirocin Combination cortisone, antibacterial, anticandidal ointment often beneficial ■ Injectable fillers

Aphthous Ulcers (Aphthous Stomatitis; “Canker Sores”)

Etiology: Idiopathic; may have genetic basis, infectious and immune mechanisms play a role. History: Common (10%–20%), often recurrent, painful mouth ulcerations. May have a prodromal stage of burning or pricking sensation of the oral mucosa immediately prior to ulcers appearing. Precipitating factors include local trauma or food hypersensitivity.

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67 Physical: Round to ovoid shallow mouth ulcers (3–8 mm) with circumscribed margins and erythematous borders. Most common on buccal & labial mucosa and edges of tongue. Investigations: Viral culture to exclude herpes infection. DDx: Behçet or Crohn’s disease, herpes simplex, pemphigus vulgaris, traumatic ulcers, neutropenic ulcers.

Management Lesions resolve in 1–2 wk w/o Tx; avoid spicy or citrus foods. Choice of therapy dependent upon severity of symptoms and frequency of recurrence. ■ symptomatic relief with topical anaesthetics (e.g., lidocaine gel/sol’n). ■ NSAIDs. ■ Topical or intralesional corticosteroids; 1–3 days of prednisone hastens/aborts attack. ■ Antimicrobial mouth rinses (e.g., tetracycline). ■ Sucralfate suspension qid to ulcers. ■ continuous debilitating episodes: oral steroids, colchicine 0.6 mg po bid to tid, or rarely, thalidomide.

Atopic Dermatitis (Atopic Eczema)

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Atopic Dermatitis (Atopic Eczema) (Continued)

Chronic inflammatory dermatosis affecting 10%—20% of children (esp. infants and young children) Etiology: Cutaneous immune dysfunction; IgE-mediated; genetics. Strong association with personal and family history of atopy (eczema, asthma, hay fever). History: Pruritus is a hallmark (“the itch that rashes”). Aggravating factors: sweating, contact sensitivity, secondary infection, wool, food allergy, stress/anxiety. Physical: ■ Acute: Erythematous, excoriated, scaling patches and plaques; more lichenification in chronic forms ■ Distribution: ■ Infant: Cheeks, forehead, scalp, extensor surfaces of extremities. ■ Child: Flexural surfaces—antecubital and popliteal fossae, wrists, ankles. ■ Adults: Hands. ■ Lesions can be secondarily infected with staphylococcal organisms: impetigo. DDx: Contact dermatitis, psoriasis, seborrheic dermatitis. Investigations: Allergy or RAST testing of little value.

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69 Atopic Dermatitis U.K. Working Party Criteria (1994)

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Basal Cell Carcinoma (BCC)

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71 Most common skin cancer derived from stem cells of epidermis. Etiology: Chronic UV exposure, radiation, immunosuppression, genetics (e.g., nevoid basal cell carcinoma syndrome). History: Persistent, nonhealing papule or nodule that ulcerates or bleeds. Common in elderly Caucasians. Physical: Pearly papule or nodule with telangiectases, rolled border; central crust or ulceration. Distributed mostly on sun-exposed areas, i.e., head and neck (85%). Variants: Cystic, superficial, nodular, sclerosing (morpheaform), pigmented. DDx: Melanoma, nevus, SCC. Investigations: Biopsy must be performed to confirm diagnosis and classify subtype.

Management ■ Advise that metastases and death are extremely rare. Vast majority cause no major problem, but should be treated. ■ Tx options depend on histological subtype and location: Liquid nitrogen cryotherapy (aggressive; requires experience), curettage & electrodessication (most common Tx), excision, Mohs micrographic surgery, imiquimod (Aldara™) cream for superficial subtype, 5-FU, CO2 laser, radiation therapy. ■ Advise on sun protection, regular TBSE.

Bullous Pemphigoid (BP)

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Bullous Pemphigoid (BP) (Continued)

Etiology: IgG produced against antigens in the dermal-epidermal basement membrane leads to subepidermal tense bullae. History: Autoimmune bullous skin disease observed predominantly in patients ⬎ 60 yr; usually self-limited over 5—6-yr period. It may be accompanied by pruritus, especially in urticarial (early) form of BP. Physical: Large tense bullae and denuded areas on erythematous or normal skin; 20% have oral lesions. Investigations: Lesional biopsy for histology and perilesional for immunofluorescence. DDx: Bullous impetigo/tinea, pemphigus (or many other autoimmune blistering conditions), drug-induced bullous disorders.

Management ■ Topical strong steroids, e.g., clobetasol cream/ungt bid (for localized disease). ■ Can use oral prednisone (0.75 mg—1 mg/kg/d) ⫹/⫺ steroid sparing agents (e.g., azathioprine, mycophenolate mophetil). ■ Methotrexate (lower doses than psoriasis; often 7.5 mg—15 mg sufficient). ■ Tetracycline (1g—2 g/d) and nicotinamide (1.5 g—2 g/d) effective in some cases.

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73 Candidiasis

Courtesy of Dr. William Gerstein Etiology: Cutaneous or mucous membrane infection caused by Candida albicans yeast. More prevalent in immunosuppressed patients, diabetics, patients who’ve had prolonged use of antibiotics, corticosteroids, or immunosuppressive agents; heat, humidity, and shear friction promote infection. History: Skin surfaces in close proximity that provide a warm and moist environment. Pruritic red rash. Paronychia and onychomycosis present as painful and red areas around the nail and can be associated with immersion of hands in water and with diabetes mellitus. Investigations: KOH microscopy of scrapings from lesions reveals mycelium & spores; confirmatory fungal culture. DDx: Eczema, psoriasis, seborrheic dermatitis. Candidal intertrigo is a common cutaneous pattern: E.g., groin and gluteal folds, the inframammary region, axilla and the interdigital spaces of the hands and feet affected. Physical: Initially vesicles, pustules, or erythematous plaques, progressing to maceration and fissuring. Central erythematous plaque often bordered by discrete pustules in a “satellite pattern.” Oral candidiasis ⫽ thrush: Chronic mucocutaneous candidiasis may be associated with autoimmune diseases and endocrinopathies.

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A-F Physical: White plaques occur on the mucosal surfaces of the mouth (thrush); lesions may be removed by scraping, yielding an erythematous base. Candida paronychia (nail infection) is often a result of chronic water exposure and trauma: Painful red swelling of periungual skin.

Management Prevention: Avoid heat, humidity, and tight-fitting clothing. Tx ■ Identify and control underlying diseases, e.g., diabetes. ■ Topical antifungals: E.g., nystatin, ketoconazole, clotrimazole, bid x 2 wk ■ Oral antifungals in extensive mucocutaneous infections: E.g., ketoconazole 200 mg po qd x 10 d. ■ Vaginal candidiasis: Single dose oral fluconazole 150 mg effective; topical & suppositories can be tried.

Cellulitis

Etiology: Soft tissue infection and inflammation caused by Streptococcus pyogenes or Staphylococcus aureus. Facial cellulitis in children is most commonly caused by Haemophilus influenzae.

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75 History: Local trauma, abrasions, and dermatoses (e.g., stasis dermatitis and tinea pedis) can be predisposing factors; drug use; impaired lymphatic drainage (e.g., lymphedema). Local pain and swelling are common. Fever, chills, and malaise may be noted. Physical: Area of spreading erythema, warmth, tenderness, pitting; associated with fever and an elevated white blood cell count. Investigations: If moderate-severe, consider: CBC&D, blood cultures, BUN, Cr, culture fluid from bulla or abscess. DDx: Erysipelas, impetigo, insect bites, stasis dermatitis.

Management Appropriate antibiotic therapy, e.g., cephalexin 250 mg po qid or cloxacillin 250 mg—500 mg po qid x 14 d. Intravenous antibiotics in severe disease, facial cellulitis, patients with underlying medical problems.

Chickenpox (Varicella)

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A-F Etiology: Varicella zoster virus (VZV) causes chickenpox; after primary infection, VZV remains dormant in sensory nerve roots for life, reactivation results in herpes zoster (shingles). History: Often pruritic. Usually mild, self-limited illness in children; more severe in adults; rarely complicated by staph/strep bacterial superinfection, pneumonia, cerebellar ataxia, encephalitis. Physical: Characteristic exanthem—Crops of erythematous macules progress to edematous papules and finally vesicles over 24—48 hr. Vesicles resemble “dew drops on rose petals.” Lesions are in different stages (polymorphous). Incubation: 10—21 d. Infectious from 4 d prior to onset of lesions to crusting of final lesion (5 d after onset). Investigations: Direct fluorescent antibody testing on fluid from vesicle base DDx: Other viral exanthema, drug eruption, herpes simplex, insect bites.

Management Prevention: Vaccine now available. Tx ■ Supportive/symptomatic treatment in children. ■ VZIG if immunocompromised or exposed neonate within 96 hr. ■ Oral antiviral therapy (acyclovir, valacyclovir, famcyclovir) in selected patient populations (ⱖ13 yr, diabetes, CF, HIV, inborn errors of metabolism, severe fulminant skin disease, & visceral involvement).

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77 Chondrodermatitis Nodularis Helicis

Etiology: Common, benign condition of the helix or antihelix of the ear in the elderly and due to persistent local pressure, e.g., from sleeping on one side. History: Very painful; awakens from sleep. Physical: Firm, tender nodule, occasionally with crust on helix or antihelix of ear. Investigations: Biopsy if unsure of diagnosis. DDx: AK, BCC, gouty tophus, KA, SCC.

Management Rarely resolves on its own. Tx ■ Relieve or eliminate pressure at site of nodule: E.g., with a pressure-relieving ear cushion. ■ Potent topical or intralesional steroids. ■ Cryotherapy. ■ Surgical options: Wedge excision of involved skin and cartilage, curettage and electrodessication.

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A-F

Contact Dermatitis

Can be divided into two main subtypes: Irritant contact dermatitis (~80%) and allergic contact dermatitis (~20%).

Irritant Contact Dermatitis (ICD) Etiology: Acute or chronic/cumulative direct nonimmunologic inflammatory reaction to toxic injury, e.g., by chemical/irritant agents. Occurs in all individuals exposed to chemicals, given sufficient exposure times and concentrations; no previous exposure necessary. History: Regular exposure to common irritants: water, soap, detergents, solvents, alcohol. Pain, burning, and stinging exceed pruritus early on. Those with history of atopic dermatitis are more susceptible.

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79 Physical: Ill-defined erythematous, scaling, papulovesicular dermatitis; chronic—scaling lichenified dermatitis. Investigations: Patch testing to rule out ACD. DDx: Dermatitis—allergic contact atopic, nummular, seborrheic, stasis; cellulitis; drug reaction.

Management Prevention: Avoid irritant exposure by use of barriers (gloves, barrier creams) and/or by using less irritating materials as substitutes. Treatment: Liberal use of nonsensitizing moisturizers (e.g., plain petroleum jelly) ⫹/⫺ topical steroids.

Allergic Contact Dermatitis (ACD) Etiology: Type IV delayed-type hypersensitivity reaction of the skin. Develops following exposure to chemicals to which the individual has been previously sensitized; prevalence varies with allergen. Common allergens: poison ivy/oak/ sumac, nickel, neomycin, bacitracin, rubber/latex, fragrances, formaldehyde. History: Detailed history of exposure to allergens, workplace or hobbies; history of pre-existing skin disease (e.g., atopic or stasis dermatitis); medications. Physical: Erythematous, scaling, papulovesicular dermatitis at sites of contact with the allergen; chronic—scaling lichenified dermatitis. Investigations: Skin patch testing (on back) to establish diagnosis (different from prick testing). DDx (ACD, ICD): Atopic or nummular dermatitis, drug reaction, scabies.

Management

■ Proper counseling on allergen avoidance, including crossreactants. ■ Acute cases: Oral antihistamines, potent topical steroids or systemic prednisone in severe cases.

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A-F ■ Patients with multiple allergies or sensitivities should be advised to test out new skin care products by applying them to the inner aspect of their arm, twice a day without occlusion, for 1 wk before applying elsewhere on the body.

Misconceptions About Allergic Contact Dermatitis (ACD) Misconceptions

In fact

Rash should quickly follow contact.

Rash is usually delayed 1—2 d and may not appear for a week after contact.

Allergy develops mainly to new substances.

Allergy can develop at any time, to any product, even after years of contact.

Allergy is dose dependent.

Allergies are not necessarily dose dependent.

If a consumer changes exposure to a product and the rash doesn’t clear, the product is not the cause.

Many products contain the same or cross-reacting antigens, and product composition can change without notification.

Contact allergy occurs only at the site of exposure to the antigen.

Although the dermatitis is often most severe at the site of exposure, dermatitis can become generalized or can be spread to distant sites (e.g., nail polish transferred to eyelids).

Negative scratch/prick testing or negative radioallergosorbent testing (RAST) as carried out by allergists rules out ACD.

Only patch testing is diagnostic.

Expensive products are less likely to be allergenic.

Cost of products does not determine its allergic properties.

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81 Cutaneous Horn

History: A clinical diagnosis of an asymptomatic conical keratotic projection resembling a miniature horn. Etiology: ⬎50% of lesions have a benign base. Common underlying lesions include: AK, BCC, SCC, SK, and wart, although many others have been reported. Physical: A hyperkeratotic papule with hornlike projection often on sun-exposed skin. Investigations: Biopsy down to base of lesion. DDx: AK, BCC, KA, SCC.

Management Tx Depends on underlying etiology, but typically cryotherapy or surgical excision.

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A-F

Cysts

Epidermoid Cyst Proliferation of epidermal cells within a circumscribed space of the dermis History: Slow growing; usually asymptomatic; tender if ruptures. Physical: Smooth & shiny mobile subcutaneous mass; cyst wall may be thin and can rupture if distended or traumatized; if the cyst contents leak into the adjacent dermis, inflammation leads to erythema and tenderness. Variants: epidermal/ sebaceous (odor), pilar/trichilemmal (odorless; scalp), milium. DDx: Lipoma; a pit or punctum can often be seen on the cutaneous surface overlying the cyst, differentiating it from lipoma. Investigations: Rarely, ultrasound or fine-needle aspiration can be performed.

Management Usually for cosmesis. Surgical excision or enucleation is definitive. Drain ruptured cysts. Occasionally intralesional cortisone is beneficial.

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83 Dermatofibroma

Benign slow-growing asymptomatic skin tumor. Etiology: Sometimes associated with a history of trauma, such as insect bite or ruptured cyst. Physical: Small (4 mm—10 mm) firm, often raised, dermal redbrown nodule; usually on legs of adults. “Dimple” sign: dermatofibroma dimples into the surrounding skin upon lateral pinching. Investigations: Biopsy if in doubt. DDx: BCC, keloid, melanoma, nevus.

Management ■ Reassurance; Tx for cosmesis. ■ Liquid nitrogen cryotherapy or intralesional cortisone can be attempted. ■ Surgical excision to subcutaneous fat. ■ Should be removed if rapidly growing.

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A-F

Dermatomyositis

Autoimmune inflammatory myopathy with systemic manifestations. History: Fatigue, pruritus, proximal muscle weakness, dysphagia. Physical: Skin findings often the initial manifestation—pink-violet eyelid rash (heliotrope) and Gottron’s papules (violaceous) over dorsal knuckles are specific cutaneous findings; also, poikiloderma in a photosensitive distribution (shawl pattern), violaceous erythema and scaling on extensor surfaces (Gottron sign), periungual and cuticular dilated telangiectases; calcinosis cutis in children. Internal malignancies

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85 associated with dermatomyositis (in adults); screening should be done (esp. ovarian ca; nasopharyngeal ca. in Asians). Investigations: Muscle enzymes (CK, aldolase) ⫹/⫺ muscle biopsy, skin biopsy, malignancy work-up. DDx: Lupus, other connective tissue disorders, lichen planus.

Management ■ R/O underlying malignancy. ■ Muscle disease: Oral prednisone (1 mg/kg/d) for 2—3 yr, steroid-sparing agents: Methotrexate, azathioprine, cyclosporine, mycophenolate mophetil, IVIG. ■ Cutaneous disease: Sunscreens, topical steroids, topical pimecrolimus or tacrolimus, hydroxychloroquine (plaquenil; 200 mg—400 mg/d). ■ Often co-managed by dermatologist and rheumatologist.

Eczema: Nummular

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A-F

Eczema: Nummular (Continued)

Common, round, and itchy form of dermatitis. Etiology: Often occurs on background of dry skin, in colder climates; worse in winter. Physical: Erythematous, coin-shaped (nummular) plaques; mostly on extremities and in elderly. Investigations: If diagnosis in doubt, scraping and KOH for tinea and skin biopsy to rule out other causes. DDx: Atopic dermatitis, contact dermatitis, psoriasis, tinea corporis.

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87 Management ■ Humidify air. ■ Avoid excessive bathing; take brief lukewarm showers; reduce use of soaps. ■ Moisturize skin after bath or shower with thick cream or ointment. ■ Potent topical steroids to nummular plaques bid x 2—3 wk. ■ Antihistamines prn if diffuse and poor sleep (use sedating type at night, e.g., hydroxyzine).

Erysipelas

Etiology: Superficial bacterial skin infection usually caused by Streptococcus pyogenes; affects lymphatics. History: May be accompanied by fever, chills, nausea, vomiting, headache, and arthralgias. Physical: Warm, swollen, erythematous plaque with sharp border; face & legs. Investigations: CBC&D, blood and wound cultures, ESR, urinalysis. DDx: Cellulitis, contact dermatitis, herpes zoster.

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A-F

Management ■ Adults: Systemic antibiotics (e.g., penicillins; erythromycin if pen. allergic) that offer coverage for both staphylococcal and streptococcal organisms for 10 d; cold compresses. Elevate & rest affected limb. ■ Children between the ages of 6 and 36 mo: Cover for H. influenzae.

Erythema Multiforme

A self-limited (1–4 wk) skin reaction pattern to a variety of stimuli. Etiology: Herpes simplex virus (cold sore) and mycoplasma are common precipitants, but often idiopathic; controversial whether drugs are triggers. History: May be accompanied by malaise and arthralgias. Physical: Classic iris or target lesions (3 rings) in a symmetrical & acral distribution (best observed on palms/soles); centers may be vesicular or dusky; Koebner phenomenon (lesions at sites of injury). Investigations: Punch biopsy; in severe cases: CBC&D, ESR, LFTs, BUN, Cr, urinalysis, electrolytes, and blood/urine/ sputum cultures. DDx: Drug eruption, lupus, urticaria.

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89 Management ■ Supportive: Antipyretics, antihistamines, analgesics, topical steroids prn. ■ If recurrent with HSV, consider treating with chronic suppressive oral antivirals & sun block for photoinduced outbreaks. ■ Less commonly: Dapsone, hydroxychloroquine, azathioprine. ■ Role of prednisone is controversial; consider use if severe pruritus and discomfort.

Erythema Nodosum

Common form of septal panniculitis that is usually a reactive skin response to an associated trigger Conditions potentially associated with erythema nodosum ■ Infections: Bacterial (e.g., streptococcal pharyngitis), mycobacterial (tuberculosis), yersinia, etc. ■ Drugs: E.g., oral contraceptives, sulfonamides ■ Sarcoidosis ■ Inflammatory bowel disease

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A-F ■ Behçet disease ■ Malignancies, esp. hematological ■ Pregnancy ■ Idiopathic History: Lesions may be associated with fever, malaise, leg edema, and arthralgia. Recurrence not uncommon. Resolution after 2—6 wk. Physical: Painful, dull, erythematous nodules 1 cm—5 cm in diameter, located on anterior lower legs of young women. No ulceration, discharge or scarring. Investigations: Thorough review of systems; CBC, urinalysis, chest X-ray, ASOT titer and throat swab (w/ streptococcal pharyngitis). DDx: Insect bite reaction, erysipelas, erythema induratum, urticaria.

Management Investigate for and treat underlying cause. Most patients benefit from bed rest, gentle support hose, applying ice or cool compresses, elevating legs, & NSAIDs. Less common Tx choices: Potassium iodide 300 mg—900 mg/d x 2—4 wk, oral prednisone, colchicine, dapsone.

Erythroderma

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91 Cutaneous reaction pattern associated with a diverse range of dermatoses. History: Chills, malaise, and fever may develop due to excessive vasodilation. Pruritus common. Physical: Generalized erythematous skin eruption involving ⬎90% of the body. May be life threatening due to generalized failure of skin functions, e.g., fluid loss through skin may result in hypotension ⫹/⫺ electrolyte imbalance. Skin infections common. Investigations: Ascertain history of potential underlying dermatosis, skin biopsies. DDx: Common cutaneous diseases that may present with or develop into erythroderma ■ ■ ■ ■ ■

Idiopathic Dermatitis (atopic, contact, or seborrheic) Psoriasis (#1 identifiable cause) Drug reaction (allopurinol, gold, carbamazepine, phenytoin) Cutaneous T-cell lymphoma (Mycosis fungoides & Sézary syndrome) ■ Pityriasis Rubra Pilaris (PRP) ■ Leukemia ■ Paraneoplastic

Management ■ Treatment: Depends on etiology—stop offending drug; cyclosporine and acitretin in psoriatic erythroderma; acitretin in PRP. Occasionally prednisone, methotrexate and azathioprine used. ■ Supportive management: Hospital admission, proper hydration, nutrition, electrolyte monitoring, cardiac monitoring, temperature support. ■ Skin care: Emollients, soaks, & compresses, mild-mod topical steroids. ■ Antihistamines for pruritus, sleep. ■ Antibiotics if any signs of infection.

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A-F

Folliculitis

Etiology: Inflammation of hair follicles due to infection, physical or chemical irritation. Often idiopathic. Most commonly bacterial infection, often due to S. aureus; Pseudomonas (“hot tub folliculitis”); Pityrosporum folliculitis; viruses and fungi rarely. History: Frequently initiated by mild physical injury to follicles, such as friction of tight-fitting garments, or by ingrown hairs in the male beard area. More common in obese & diabetics. Ask about hot tub exposure. Physical: Superficial pustules and/or papules in the distribution of hair follicles; affects—face, scalp, chest, back, thighs, and buttocks. Investigations: Swab for culture and sensitivity of opened pustules; KOH prep; biopsy. DDx: Acne, insect bites, miliaria, scabies.

Management ■ Eliminating the offending agent(s): Antibiotics if bacterial, antifungals if Pityrosporum, antivirals if herpes, & symptomatic management if Pseudomonas.

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93 ■ If fails therapeutic antibacterial trial, consider more extensive work-up (cultures, KOH, biopsy). ■ Shower with antibacterial soaps/washes. ■ Topical antibacterials: Fucidin, mupirocin, erythromycin. ■ Systemic antibacterials: E.g., cloxacillin x 7—10 d or antifungal preparations (depending on culture). Occasionally long-term tetracycline or its derivatives required.

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G-M

Granuloma Annulare (GA)

Common benign inflammatory granulomatous dermatosis of unknown etiology. History: Usually asymptomatic; most pts. ⬍30 yr Physical: Papules and annular plaques with central depression; commonly on dorsae of hands, feet, elbows (acral). Variants: Arcuate dermal erythema, localized, generalized, micropapular, patch, perforating, & subcutaneous. Generalized (15%; older pts.; poorer response to Tx) and perforating GA (5%; small umbilicated papules) may be associated with diabetes mellitus (controversial). Course: Usually self-limiting; resolves within 2 yr in 75% of patients; high recurrence rate. Investigations: Biopsy to confirm diagnosis. DDx: Erythema elevatum diutinum, lichen planus, sarcoidosis, tinea corporis.

Management ■ Reassurance & clinical observation since benign & selflimited. ■ Mainly for cosmetic purposes. ■ Localized GA: intralesional or potent topical steroids, cryotherapy. ■ Generalized GA: PUVA, prednisone, pentoxifylline, oral retinoids.

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95 Hand, Foot, and Mouth Disease

Courtesy of Dr. Henry Foong Self-limited (7—10 d) systemic infection usually caused by coxsackievirus A16 affecting young children. Highly contagious, and spreads by direct contact. History: Often accompanied by low-grade fever, malaise, and sore mouth; refusal to eat. Physical: Multiple small vesicles with red halo on fingers and toes, ulcerative oral lesions (90%). Investigations: Clinical diagnosis; can culture virus from mucosal or cutaneous lesions. DDx: Aphthous stomatitis, chickenpox, erythema multiforme, herpes simplex.

Management ■ Symptomatic: Topical anesthetic gel (lidocaine). ■ Antipyretics: E.g., acetaminophen, ibuprofen. ■ Ensure adequate fluid intake.

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G-M

Hemangiomas (Infantile; “Strawberry Hemangioma”)

Benign vascular tumor of endothelial cells. History: 40% present at birth; remainder develop within 8 wk; 60% on head & neck. Rapid growth phase at 4—8 wk until 6—9 mo; spontaneous regression begins at 18—24 mo; 50% involute by 5 yr, 90% by 9 yr. Physical: Divided into 3 types—Superficial (red and papular), deep (blue-gray and nodular), and mixed; residua: hypopigmentation, telangiectases, scarring (if ulcerated), redundant tissue. Complications: Obstruction depending on location (e.g., vision, breathing), ulceration, infection. Investigations: Consider MRI or U/S if in beard, oral or periocular areas involved. DDx: Congenital hemangioma, vascular or lymphatic malformation.

Management ■ Indications for treatment: Kasabach-Merritt syndrome; high output failure, obstruction of vital function (feeding, respiration, passage of urine/stool); nasal, auditory, or ocular obstruction; ulceration; cosmetic disability. ■ Observation and reassurance in most cases.

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97 ■ Referral to subspecialist (e.g., ophthalmology, ENT) if local obstruction. ■ Prednisone 2 mg—4 mg/kg/d until 1 yr; occasionally intralesional steroids. ■ Laser (pulsed dye), especially if ulcerated. ■ Less commonly, excision; rarely interferon alpha. ■ Newer treatment options may be considered: potent topical steroids, imiquimoid 5% cream, becaplermin gel 0.01% (for ulcerated hemangiomas). ■ When pt. older, may need plastic surgery or laser for redundant tissue and persistent telangiectases, respectively.

Henoch-Schönlein Purpura (HSP)

Courtesy of Dr. Henry Foong Common small vessel vasculitis of childhood with annual incidence of 20 per 100,000, highest in boys between 4 and 6 yr. Frequently associated with a URTI; peak occurrence in winter & fall. History: 2—3-wk history of fever, headache, myalgias, arthralgias, and abdominal pain may precede rash. Physical: Purpuric papules on buttocks, legs, & extensor extremities. Usually benign and self-resolving condition, lasts 6—16 wk.

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G-M ■ Classic tetrad of symptoms: Cutaneous purpura (100%), arthralgias/arthritis (~80%), abdominal pain (~70%), and gastrointestinal bleeding (33%). ■ Renal involvement observed in 25%—50% of patients, heralded by asymptomatic microscopic hematuria and proteinuria, but is usually mild and self-limiting; with increasing age at presentation, nephrotic syndrome, hypertension, and acute renal failure may occur. ■ Complete recovery in 94% of children and 89% of adults. Investigations: Skin biopsy; early DIF helpful—reveals IgA deposits in walls of small blood vessels; U/S & x-ray for GI symptoms; occasionally renal biopsy needed; blood work: CBC&D, BUN, Cr, urinalysis, complement, ASOT. DDx: Erythema nodosum, LCV, lupus

Management ■ Mostly supportive, adequate hydration, NSAIDs to treat arthralgias. ■ Close follow-up of renal status w/ repeat urinalyses and renal function tests, referral to nephrologist if renal complications occur. ■ Corticosteroids (most evidence for abdominal and joint symptoms), dapsone, cytotoxic agents and IVIG might be of benefit.

Herpes Simplex (HSV)

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99 Herpes Simplex (HSV) (Continued)

HSV-1 Common viral infection affecting the oral mucocutaneous surface. HSV-1 is most commonly associated with oral-facial lesions. History & Physical: Most patients have subclinical primary episode, others experience primary gingivostomatitis, i.e., 3—5 d of fever, malaise, lymphadenopathy, oral mucosal erosions ■ Recurrent HSV-1 infection (herpes labialis) after primary infection may be reactivated by a number of triggers: stress, fever, UV light, trauma, menstruation; burning and itching precede appearance of grouped umbilicated vesicles on erythematous base, herpetiform arrangement, commonly on the vermilion border of the lip. face; crust over in 7–10 d. DDx: aphthous stomatitis, hand-foot-and-mouth disease, impetigo

HSV-2 Common viral infection affecting the genital mucosa, although oral mucocutaneous involvement reported with increasing prevalence. History & Physical: Most are sexually transmitted; primary episodes more severe, with painful erosive balanitis, vulvitis, or vaginitis; recurrent infections are milder or subclinical.

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G-M DDx: Chancroid, syphilis, fixed drug eruption. Investigations: Direct fluorescent antibody testing of fluid from base of vesicle; viral culture or PCR from lesion swab; Tzanck smear shows multinucleate giant epithelial cells. Herpetic whitlow ⫽ herpes of fingertip; Herpes gladiatorum ⫽ herpes among wrestlers & rugby players; Eczema herpeticum ⫽ eczema secondarily infected with herpes.

Management ■ Immunocompetent patients, 1st or occasional episode: Tx often supportive; can treat if severe or disseminated. ■ Within 72 hr, oral antiviral therapy may be instituted to reduce pain, viral shedding, and time to healing: Acyclovir, famciclovir, valacyclovir can be used with dosage depending on whether 10 vs 20 episode. ■ If severe, frequent (⬎6/yr) recurrences, consider chronic suppressive antiviral therapy. ■ Consider antiviral prophylaxis prior to skiing or tropical vacations (& sunscreen), extensive dental work, or cosmetic procedures on the face. ■ Topical antivirals of no benefit.

Herpes Zoster (“Shingles”)

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101 Etiology: Varicella zoster virus (VZV) causes chickenpox; after primary infection, VZV remains dormant in sensory nerve roots for life, and reactivation results in herpes zoster (shingles). Reactivation may be idiopathic, but may occur with immunosuppression or stress. Increased incidence with increasing age; more common in HIV & hematologic malignancy. History: Pain/tenderness in a unilateral dermatomal distribution often precedes rash. Physical: W/i 3—4 d of onset of symptoms, clusters of erythematous papules and vesicles develop in a dermatomal distribution (thoracic ⬎ cranial ⬎ lumbar); new groups of lesions continue to appear over several days, eventually followed by crusting and desquamation over a 2—4-wk period. Generalized zoster: Lesions involve several nonadjacent dermatomes and cross the midline. Complications: Postherpetic neuralgia (PHN), scarring, secondary bacterial infection. PHN occurs in 50% of pts ⬎ 60 yr, & is present at 1 yr in 10%—25%; characterized by shooting or burning pain in the previously involved sites; more common in older patients and when the trigeminal nerve is involved. Investigations: Diagnosis is mostly clinical; if unsure, same work-up as for chickenpox and biopsy can be helpful. DDx: VZV, herpes simplex, folliculitis.

Management ■ If identified within 72 hr, oral antiviral therapy can speed healing and decrease pain (PHN): Acyclovir 800 mg 5 x d x 7 d, famciclovir 500 mg tid x 7 d, or valacyclovir 1000 mg tid x 7 d. ■ If tip of nose involved/V1 dermatome facial involvement: Urgent ophthalmology consult—Ocular involvement can lead to blindness. ■ PHN: Difficult to manage, best prevented by immediate antiviral therapy; analgesics, topical lidocaine, capsaicin, narcotics, nerve blocks, gabapentin, tricyclic antidepressants may be helpful; pain clinic referral. Prednisone occasionally used in elderly in addition to antivirals for herpes zoster (controversial).

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G-M

Hidradenitis Suppurativa

Etiology: Chronic recurrent inflammatory condition wherein hair follicles are occluded and become secondarily infected. Associated with obesity, diabetes, and smoking; genetic and hormonal components. History: Pain, odor, and drainage affecting axillae and/or groin. Physical: Comedones, pustules, and nodules, abscesses, sinuses, and scarring. Severe form associated with acne conglobata, pilonidal sinus, & dissecting cellulitis of scalp. Investigations: Clinical diagnosis; can swab for bacterial cultures. DDx: Folliculitis, infected cysts, inflammatory bowel disease.

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103 Management ■ Distressing condition with no satisfactory treatment. ■ Topical and systemic antibiotics (e.g., clindamycin and tetracycline), intralesional corticosteroids, hormonal therapy, retinoids (e.g., isotretinoin, acitretin). ■ Daily cleansing with antibacterial soaps. ■ Female patients benefit from antiandrogen therapy such as cyproterone acetate or spironolactone. ■ Surgery is required for more recalcitrant cases and can be curative. ■ Encourage patients to quit smoking and lose weight.

Hyperhidrosis

Etiology: Excessive sweating, either generalized or focal (e.g., palmar, palmoplantar, axillae), and affecting 2%—3% of general population; most common in adolescence and young adults. Generalized hyperhidrosis can be associated with underlying systemic disorder, e.g., infectious (e.g., TB), endocrine, or neurologic; focal hyperhidrosis often idiopathic. History & Physical: Diagnostic criteria for primary focal idiopathic hyperhidrosis. ■ Focal, visible, excessive sweating of at least 6 mo duration without apparent cause with at least 2 of the following characteristics:

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G-M ■ Bilateral and relatively symmetrical sweating. ■ Frequency of at least 1 episode per wk. ■ Impairment of daily activities. ■ Age at onset ⬍ 25 yr. ■ Positive family history. ■ Cessation of sweating during sleep. Investigations: Starch iodine test can be used to outline the area of excessive sweating. DDx: Thyrotoxicosis, medication-induced hyperhydrosis, pheochromocytoma.

Management Important to rule out systemic causes—infections, malignancy (ask about night sweats). Topical: Aluminum chloride hexahydrate solution in ethanol (e.g., Drysol®), glycopyrrolate iontophoresis. Systemic: Anticholinergics (e.g., Robinul® 1 mg bid—tid), diltiazem, clonidine, Botulinum toxin (Botox®) injections— very effective; can last 6—12 mo. Surgery: Endoscopic thoracic sympathectomy, subcutaneous liposuction.

Impetigo

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105 Etiology: Superficial infection of the skin caused by Staphyloccocus aureus or group A beta-hemolytic Streptococcus (GABHS). Can be primary or secondary, e.g., impetiginization of an underlying dermatosis, as in atopic dermatitis, insect bites, scabies, and viral infections. History: Spread by direct contact and most common in children. Highly contagious. Usually asymptomatic. Physical: Superficial pustules covered by moist, honey-colored crusts; lesions may be localized or extensive; face and extremities commonly affected. Pt. nontoxic. ■ May see vesicles and bullae with yellow-brown crust (bullous impetigo), typically caused by phage group II of S. aureus. Course: Generally self-limited; risk of post-strep glomerulonephritis, but not rheumatic fever. Investigations: Culture and sensitivity. DDx: Herpes simplex, eczema, contact dermatitis, scabies.

Management ■ Localized: Topical antibiotics (mupirocin or fusidic acid tid). ■ Generalized: Oral cephalexin, cloxacillin, or erythromycin x 7—10 d. ■ Saline compresses prn to remove crust. ■ Consider intranasal mupirocin (bid x 5—7 d) if recurrent.

Keratoacanthoma (KA)

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G-M Skin tumor, possibly an early or abortive phase of SCC; rare association with Muir-Torre syndrome. History: Rapid growth (over 2—6 wk) and may resolve spontaneously. Physical: Firm, dome-shaped, crater-like nodule most common on sun-exposed skin of older adults. DDx: AK, cutaneous horn, SCC. Investigations: Excisional or deep incisional biopsy.

Management ■ Excision, curettage, and electrodessication. Uncommonly: Aggressive cryotherapy, radiotherapy, intralesional therapy (e.g., 5-FU, bleomycin).

Keratosis Pilaris (KP)

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107 Common, benign disorder of keratotic follicular papules. Etiology: Genetic component more common in atopic and xerotic patients, and worse in winter. History: Usually asymptomatic, with occasional pruritus, improves with age. Physical: Hyperkeratotic follicular papules (⫹/⫺ erythema) typically distributed over the outer aspects of upper arms and thighs, less commonly the face, forearms, & buttocks. Investigations: Clinical diagnosis. DDx: Atopic dermatitis, folliculitis, lichen spinulosus.

Management Treatment often disappointing in all but mild cases. Tx choices: Lactic acid (e.g., Lac-Hydrin lotion®), urea-based emollients, salicylic acid in urea, tretinoin. Mild cortisone can be added if erythema present.

Lichen Planus (LP)

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G-M

Lichen Planus (LP) (Continued)

Acute or chronic inflammatory disorder affecting the skin, mucous membranes, and nails (5%—10%). Etiology: Likely an immunologically mediated reaction; oral erosive lichen planus associated with hepatitis C. History: Pruritus common; oral lesions may or may not be symptomatic. Ask about Hep C risk factors (e.g., transfusions, IV drug use) for oral-erosive LP. Physical: 7 P’s—Planar (flat-topped), pruritic (intense), purple, polygonal, papules, penile (commonly affected), prolonged course (up to 18 mo; longer in some cases); distributed on flexor surfaces, penis (glans), mouth (lacy white patches or erosions—Wickham striae). Many clinical variants reported. Koebner phenomenon ⫽ appearance of lesions at sites of trauma. Course: May resolve spontaneously or have chronic course (esp. oral LP); increased risk of oral SCC in oral LP. DDx: Drug reaction, pityriasis rosea, psoriasis Investigations: Skin biopsy if unsure of diagnosis.

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G-M Investigations: Biopsy if SCC suspected. DDx: Lichen planus, morphea, vitiligo.

Management Extragenital LS&A: Often no treatment; topical steroids or phototherapy can be tried. Genital LS&A: Ultrapotent topical corticosteroids, e.g., clobetasol, eventually tapered; can try topical tacrolimus or pimecrolimus as maintenance.

Lipoma

Slow-growing, common, benign tumor of fatty tissue in 1% of population. Several uncommon associated syndromes include lipomas. History: Usually asymptomatic; slow growth. Physical: Mobile and compressible soft subcutaneous mass; commonly on trunk. Sacrococcygeal lipoma may be a marker for spinal dysraphism. Investigations: Clinical diagnosis; uncommonly, imaging studies or biopsy. DDx: Cyst, DF, leiomyoma

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111 Management Excision or liposuction for cosmesis; rarely painful.

Lupus Erythematosus

Etiology: Heterogeneous autoimmune disease resulting from the interplay of genetic, environmental, and hormonal factors. F ⬎ M. History & Physical: Spectrum of disease varies from limited cutaneous involvement to severe systemic disease.

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Systemic Lupus Erythematosus (SLE): 1997 Update of the 1982 ACR Revised Criteria

112

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113 Management LE-specific skin manifestations are divided into 3 categories (other less common forms exist as well).

Clinical Acute cutaneous LE

Subacute cutaneous LE

Classic “butterfly” malar rash. Often association with anti-dsDNA Ab and lupus nephritis.

Two subtypes: Annular or papulosquamous presentation. Often associated with anti-Ro Ab. Chronic cutaMost often in neous/discoid head/neck area: LE Atrophic inflammatory plaques. Can lead to scarring alopecia.

Comment Evaluate for evidence of systemic disease. Hydroxychloroquine. Systemic steroids (0.5 mg–1 mg/kg/d) ⫹ steroid-sparing agents (azathioprine, methotrexate, mycophenolate mophetil). Sun protection. Corticosteroids (topical, intralesional) and hydroxychloroquine.

5%–10% will get systemic disease Tx: Photoprotection, topical or intralesional steroids, hydroxychloroquine

Other important variants of lupus: Drug-induced lupus, lupus profundus, neonatal lupus.

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115 Investigations: Diagnosis requires clinicopathologic correlation; often multiple skin biopsies needed before diagnosis made. DDx: Eczema, neurodermatitis, parapsoriasis.

Mycosis fungoides (MF) The most common clinicopathologic subtype of primary cutaneous T-cell lymphoma (CTCL).

Management Choice of therapy and management setting depends on stage of disease: “stage-directed therapy”

Overview of Mycosis Fungoides Therapies Skin-directed Therapies Topical therapies Steroids (mid to strong potency) Topical chemotherapy ■ Nitrogen mustard ■ Carmustine (BCNU) Bexarotene 1% gel Imiquimod 5% cream Phototherapy: PUVA, BB/NB-UVB, UVA-1 Radiation therapy Local x-ray therapy Electron Beam Therapy

Systemic Therapies Biological/immune therapies Bexarotene, Acitretin Denileukin Diftitox Interferon Extracorporeal photopheresis (ECP) Monoclonal antibodies Cytokine therapy Chemotherapy Methotrexate, gemcitabine Pentostatin and purine analogues Combination chemotherapy Bone marrow/stem cell transplantation

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Melanoma

Etiology: Melanocyte-derived skin cancer. May arise within a previously existing nevus or dysplastic nevus, but ~70% arise de novo. History: Risk factors ■ Fair complexion: Red/blonde hair, blue/green eyes, tendency to freckle and burn. ■ Sun exposure, particularly blistering sunburns during childhood. ■ Personal or family history of melanoma; Genes involved in some cases: CDKN2A, BRAF. ■ Giant congenital melanocytic nevi or multiple dysplastic nevi.

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117 Physical: Pigmented macule or plaque with some or all of the following features (ABCDE of melanoma): Asymmetry, Borders (irregular), Color variegation, Diameter (⬎6 mm), Evolution (lesion change by history). Classically divided into subtypes based on clinical and histopathologic features: 1. Superficial spreading malignant melanoma—60%—70% of melanomas. 2. Nodular melanoma. 3. Acral-lentiginous melanoma—Most common form in blacks, Asians, and Hispanics, mostly on volar skin of the palms or soles and the nailbeds. 4. Lentigo maligna melanoma—Develops from a lentigo maligna, usually on the face of elderly, slow-growing. 5. Amelanotic melanoma—Pink-red. 6. Rare variants. Most common sites of local and/or regional metastases— Draining lymph node basins and the skin between the primary site and the lymph nodes; most common sites of systemic metastases—Lung, liver, brain (#1 cause of death), bone, and gastrointestinal tract. Investigations: Dermoscopy (ABCD rule or 7-point checklist; requires expertise); excisional biopsy if melanoma is suspected. ■ Most important prognostic indicator is maximal thickness of tumor invasion on biopsy (Breslow depth in mm). DDx: BCC, blue or dysplastic nevus, SK.

AJCC 2002 Revised Melanoma Staging

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119

Reprinted with permission: Balch CM, et al. Final version of the American Joint Committee on Cancer staging system for cutaneous melanoma. J Clin Oncol. 2001 Aug 15;19(16):3635-48.

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Management Wide surgical excision, based on Breslow depth: 5 mm for melanoma in-situ; 1 cm for melanoma ⬍1 mm; 2 cm for melanoma ⬎1 mm. Sentinel lymph node biopsy depending on current guidelines. Adjuvant high-dose interferon & IL-2 may provide benefit for metastatic disease. Perfusion chemotherapy for extremity melanoma. Radiation—symptomatic. Melanoma vaccines being studied; patients with metastases should be referred for clinical trials.

Melasma

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121 Etiology: Acquired brown macular hyperpigmentation, mostly on face, from exposure to sunlight. Can be associated with pregnancy (“mask of pregnancy”), oral contraceptives, menopause. History: Mostly females, asymptomatic, often starts in pregnancy, worsens in summer. Physical: Well-demarcated, hyperpigmented macules, mostly on the malar prominences, forehead and mandible. Investigations: Wood’s lamp exam accentuates the epidermal pigment. DDx: Addison disease, ephelides/freckles, postinflammatory hyperpigmentation.

Management ■ Daily sun protection is essential with high SPF and broadbrimmed hat; sun blocks preferred. ■ Hydroquinone (2% OTC; 4% by Rx) are most commonly used—Azelaic acid; tretinoin. ■ Kligman or modified Kligman formula combines a hydroquinone with a mild cortisone and tretinoin. ■ Chemical peels. ■ Lasers occasionally used.

Molluscum Contagiosum

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G-M Etiology: Self-limited viral infection of skin caused by poxvirus (MCV) affecting mainly children. Immunocompromised patients (e.g., HIV) may develop more widespread and larger lesions. History: Asymptomatic; occasional perilesional pruritus. Physical: 2- to 6-mm flesh colored, dome-shaped, umbilicated pearly papules; most common affected sites—trunk and face of children, genitals/inner thighs of sexually active adults. Course: Lesions typically involute spontaneously within 9-12 mo; may develop adjacent eczema (in 10%). Investigations: Clinical diagnosis, biopsy if uncertain. DDx: BCC, milia, other infection, warts.

Management ■ ■ ■ ■ ■ ■ ■ ■ ■

Observation. Liquid nitrogen cryotherapy. Curettage; may be uncomfortable. Papule incision with a scalpel blade or at home sharp fingernail and expression of contents. Topical cantharidin: Blistering (intentional) will occur; apply with wooden end of cotton swab and cover with tape for 30 min, then wash off with soap and water; ideal in children. Imiquimod cream. Tretinoin cream. In children with widespread involvement, may consider oral cimetidine (40 mg/kg/d x 2 mo). Testing for other STDs recommended in adults with lesions in the genital area.

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123 Nevi

Melanocytic Nevi (Moles)

)

■ Benign growths composed of nests of melanocytes. ■ More common in light/fair skin. ■ First appear in childhood as flat brown macules, evolve during adulthood into dome-shaped and fleshy papules or nodules with loss of pigmentation. ■ Divided into various subtypes: Acquired melanocytic nevi, Spitz nevi, blue nevi. ■ Many nevi regress in late adulthood. ■ Need monitoring, biopsy if melanoma suspected.

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N-S Congenital Nevi

■ Present at birth or become apparent during infancy. ■ Often larger than typical melanocytic nevi and have associated hair. ■ Need monitoring, biopsy if changing or if melanoma suspected. ■ Small ⫽ ⬍1.5 cm; medium ⫽ 1.5 cm— 19.9 cm; large ⫽ ⬎20 cm. ■ Giant congenital nevi associated with increased melanoma risk.

Dysplastic Nevi (Atypical Nevi, Clark’s Nevi)

■ Nevi with irregular outline, variable pigmentation, indistinct borders, and often ⬎6 mm. ■ Multiple dysplastic nevi herald an increased risk for developing melanoma. ■ Need careful monitoring, biopsy if change in size/color.

Ephelides (Freckles)

■ Small brown macules on sunexposed skin; more common in faircomplexioned. ■ Darken in response to the sun and fade with UV abstinence. ■ No risk of melanoma if diagnosis certain.

Lentigines (Solar Lentigines, Simple Lentigines, “Liver Spots”)

■ Occur in response to sunlight and persist even in absence of sunlight. ■ Vary in color from tan to dark brown, and can be up to 1 cm in diameter. ■ Location: Dorsal hands and face.

Spitz Nevus

■ Smooth-surfaced, firm, round, brown to pink-red papule usually developing in childhood. Often on face. ■ Benign, but histologically can be confused with melanoma.

DDx: Melanoma, pigmented BCC, SK.

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125 Management Surgical excision if malignancy suspected.

Onychomycosis (Tinea Unguium)

Etiology: Dermatophyte infection of nail plate, often associated with tinea pedis. Less commonly due to yeasts and nondermatophyte molds. History: Change in nail color and more brittle; usually asymptomatic. Physical: Yellow discoloration, thickening, nail dystrophy, subungual hyperkeratosis, onycholysis. Toenails ⬎ fingernails. Patterns include the distal subungual form (most common), the proximal white subungual form (may be a sign of HIV disease), and the white superficial form. Investigations: 20% KOH direct microscopy, nail clipping/ scraping for culture. DDx: Nail psoriasis or trauma, eczema, lichen planus.

Management ■ Topical antifungals much less effective. Ciclopirox (Penlac®) nail lacquer may be tried if po Tx not an option. ■ Important to culture fungus prior to initiating oral Tx

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N-S ■ Terbinafine (Lamisil) 250 mg po qd x 6 wk for fingernails, x 12 wk for toenails; itraconazole (Sporanox) 200 mg po bid x 7 d, then 3 wk off—2 pulses for fingernails, 3 pulses for toenails. ■ Other less common options: Griseofulvin (esp. in kids), fluconazole. ■ Hepatotoxicity and leukopenia are rare side effects of terbinafine use, some check baseline and monitor CBC and LFTs during Tx; itraconazole—mostly hepatotoxic S/E. ■ Educate patients that due to slow rate of new nail formation, it may take many months after treatment to see clinical improvement.

Paronychia

Etiology: Inflammation around nail due to Staphylococcus aureus, Streptococcus, or Candida albicans (chronic). History: Often painful and tender skin around nails. Physical: Periungual swelling and erythema; tenderness to palpation. Investigations: Usually clinical; Gram staining, KOH prep, or Tzanck smear to confirm infectious etiology. DDx: Contact dermatitis, cellulitis.

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127 Management ■ Avoid exposure to excessive moisture. ■ Rule out offending drugs (e.g., retinoids, protease inhibitors). ■ Potent topical steroids; less effective are topical or systemic antifungals in chronic paronychia. ■ Topical or systemic antimicrobials. ■ Incision and drainage if acute and tense subcutaneous collection.

Pediculosis (Lice)

Courtesy of Dr. Art Huntley Etiology: Infestation by wingless, 6-legged insects (Pediculus humanus & Phthirus pubis). Spread by direct contact or through fomites (e.g., clothing, bedding). History: Symptoms vary from none to extreme pruritus. Physical: Pediculosis capitis (head louse) Gray-white nits/eggs or lice firmly adhere to hair shaft; postauricular and occipital regions commonly affected; children ⬎ adults. Pediculosis pubis (crab louse) Eyelashes and pubic hair may be affected; usually transmitted by sexual contact; nits seen on hair, red excoriated skin. Body lice Infest individuals with poor hygiene or those living in crowded conditions; eggs commonly found along seams of clothing. Investigations: Magnifying glass—assisted observation of nits or mature lice. DDx: Impetigo, insect bites, scabies.

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Management ■ Head lice: Wash hair, rinse, and towel dry; then apply permethrin cream (Nix®, Elimite®) rinse for 10 min and rinse out; repeat in 7 d. ■ Pyrethrin, malathion, crotamiton, petrolatum may be used; latter rubbed into hair to suffocate lice. ■ For pediculosis pubis—affecting eyelashes, apply petrolatum to eyelashes bid—tid x 10 d. ■ Nits may be removed with vinegar soaks (vinegar:water 1:1) and a fine-toothed comb. ■ Soak combs and brushes in permethrin shampoo for 10 min or boil. ■ Bedding, clothing, and head gear should be washed and heatdried; environment should be vacuumed; unwashable items can be sealed in plastic bags for 2 wk. ■ Contacts should be treated similarly. ■ Ivermectin (oral) increasingly used in resistant or complicated cases of lice & scabies.

Pemphigus Vulgaris

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129 Etiology: IgG produced against epidermal desmoglein 1 and 3, leading to acantholysis and intraepidermal bullae. History: Serious and uncommon autoimmune blistering disease with peak prevalence at 50—60 yr of age. Painful skin and/or oral mucosae; pruritus uncommon. Physical: Flaccid blisters or bullae, or residual erosions; mouth often involved—Mouth ulcers & odor often initial presentation (60%); healed lesions don’t scar, but leave hyperpigmented patches. Variants: Pemphigus foliaceus, pemphigus vegetans, fogo selvagem (S. America), pemphigus erythematosus, paraneoplastic pemphigus. Nikolsky sign: Rubbing the skin in unaffected site induces lesion. Asboe-Hansen sign: Blister extends with lateral finger pressure. Investigations: Lesional biopsy for histology and perilesional for immunofluorescence. DDx: Bullous pemphigoid, linear IgA bullous disease, pemphigus foliaceus.

Management ■ Requires management by an experienced physician. ■ May need hospital admission (often require burn unit care). ■ Prednisone high-dose initially (⬎1 mg/kg), then taper; add bisphosphonates, calcium, Vitamin D to protect bones. ■ Steroid-sparing agents started early & help control disease while tapering prednisone: azathioprine, mycophenolate mofetil, methotrexate, cyclophosphamide, IVIG. ■ Antibiotics if secondarily infected. ■ Symptomatic oral treatment (viscous lidocaine, diphenhydramine elixir).

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Perioral (Periorificial) Dermatitis

Etiology: Inflammatory acneiform skin condition exacerbated by potent or chronic steroid application; may be related to irritation or allergy from ingredients (e.g., detergents) in creams. History: Affects mainly females, 15—40 yr who complain of a burning sensation and tightness. Physical: Erythematous macules, papules, and plaques coalescent on perioral, perinasal, and/or periorbital skin. Investigations: None. DDx: Acne, contact dermatitis, rosacea.

Management Avoid steroids on face (discontinue, or wean). Topical: Metronidazole gel or cream bid; topical tacrolimus or pimecrolimus can be tried to wean off steroid. Systemic: Tetracycline 500 mg po bid helpful for papulopustular lesions.

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131 Pityriasis Rosea

Acute, self-limited papulosquamous inflammatory skin exanthem in 15—40 yr. Etiology: Possibly triggered by human herpes virus 7. History: May be pruritic or asymptomatic; preceding URTI or mild constitutional symptoms; larger “herald” patch with central clearing, followed 5—10 d later by trunk lesions. Physical: Scaly pink-erythematous plaques; predominantly trunk affected, in “Christmas-tree” pattern. Course: Self-resolving in 6—8 wk. Investigations: Clinical; scraping for KOH (R/O tinea) or order RPR (R/O syphilis), or skin biopsy if uncertain. DDx: Eczema, psoriasis, tinea corporis, 20 syphilis, seborrheic dermatitis.

Management ■ Reassurance is key. ■ Symptomatic management of pruritus (e.g., mild topical steroids, antihistamines prn). ■ Light therapy (e.g., UVB) may help hasten resolution and relieve pruritus.

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Pityriasis Versicolor (Tinea Versicolor)

Etiology: Common superficial cutaneous fungal infection caused by Malassezia furfur or globosa yeast. History: Usually asymptomatic, young adults typically affected; commonly recurs; more common in hot and humid environments. Physical: Round to oval macules and patches on the trunk; different colors: White, orange-brown, dark-brown; very fine scale; postinflammatory hypopigmentation is often noted rather than initial erythema. Investigations: KOH test reveals diagnostic “spaghetti & meatballs” (hyphae & spores); Wood’s lamp shows yellow-brown fluorescence. Skin biopsy if diagnosis uncertain. DDx: Tinea corporis, vitiligo, psoriasis.

Management ■ Topical or systemic treatment. ■ Nizoral shampoo (ketoconazole 2%) applied onto dampened trunk skin, lathered for 5 min before rinsing, x 3 d.

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133 ■ Topical selenium sulfide 2.5% shampoo applied for 15 min x 3 d. ■ Topical nizoral cream 2% (ketoconazole) bid x 2 wk. ■ Systemic ketoconazole 200 mg po qd x 5—7 d or fluconazole 400 mg x 1. Postinflammatory hypopigmentation may persist for 6—12 mo. ■ Even with treatment, tendency to recur in summer. ■ Zinc pyrithione soap lather may be applied to the body 1—3 times weekly for prevention.

Psoriasis

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N-S Common (1%—2%), chronic, recurrent inflammatory skin disease with unpredictable course. Etiology: Genetic & environmental factors; abnormal epidermal differentiation and hyperproliferation initiated and maintained primarily by T-cells. History: Visible itchy red plaques with increased skin scaling and peeling. May have joint pain. May have preceding URTI. Worsened by smoking, alcohol, & stress. Physical: Characteristic erythematous plaques with silvery-white scale; distributed over extensor surfaces (elbows, knees), scalp, sacrum, and other sites, Nail psoriasis: Pitting, thickening, “oil-drop,” lifting of nail plate off of distal nail bed (onycholysis). Koebnerization ⫽ new lesions occur at sites of skin trauma (as with lichen planus). Geographic tongue occurs in 10% of patients with psoriasis (see Fig. 2—1). Variants: Vulgaris (#1), palmoplantar, guttate (may follow streptococcal pharyngitis), erythrodermic, pustular (generalized ⫽ von Zumbusch type), inverse (affects folds & flexor surfaces). Drugs may precipitate or exacerbate psoriasis: Antimalarials, clonidine, indomethacin, iodine, lithium, NSAIDs, quinidine, some beta-blockers, steroid withdrawal, and terfenadine. In ~10%—20%, may be associated with psoriatic arthritis, most commonly of the small joints of the hands and feet; requires systemic Tx. Investigations: Clinical diagnosis; skin biopsy if uncertain. DDx: (Plaque psoriasis): Drug reaction, eczema, lichen planus, pityriasis rubra pilaris.

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135 Management Overview of Psoriasis Therapy Therapy

Mechanism of Action

Comments

Inhibits DNA synthesis, cell turnover.

Potency & vehicle selected based on body site. Stains and irritates normal skin.

Topical Steroids 5%—10% LCD (tar) Anthralin Salicylic acid 3%—10% Calcipotriol (Dovonex) Tazarotene (retinoid) Emollients

Increases cell turnover. Keratolytic. Vitamin D3 analogue.

Retinoid (RXR receptor).

Systemic Methotrexate

Cyclosporine

Acitretin

Folic acid antagonist that inhibits DNA synthesis & causes immunosuppression. Immunosuppressant that inhibits IL-2 production & thus reduces T-cell proliferation. Inhibits cell replication by modulating cellular differentiation within the epidermis.

Bone marrow and hepatic toxicity.

Renal toxicity, hypertension.

Preferred for palmoplantar or pustular psoriasis. Use in males & postmenopausal females.


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Overview of Psoriasis Therapy (Continued) Therapy

Mechanism of Action

Comments

Interferes with DNA synthesis, decreases cellular proliferation, and induces apoptosis of cutaneous lymphocytes leading to localized immunosuppression. ⫹⫹ Expensive.

Skin cancer development, photoaging.

Alefacept

Fusion protein of Fc receptor of human IgG1 and LFA3.

Efalizumab

Humanized monoclonal antibody to CD11a; blocks LFA-1/ ICAM interaction Fusion protein directed against soluble TNFa.

IM; when effective, long remissions; monitoring of CD4 q wk; slow onset. SC; rapidly effective, but rebound; risk of thrombocytopenia

Phototherapy UVB or PUVA

Newer Biological Agents

Etanercept

Infliximab

Chimeric monoclonal antibody against TNFa.

Adalimumab

Fully humanized antiTNF monoclonal antibody.

SC; effective for psoriasis & psoriatic arthritis; rapid onset; no monitoring; use ⫹/- MTX. IV; Fast onset and very effective; must do PPD; infusion reactions. SC; newest of the biologics, still being studied.

Note TNF drugs avoid or use with caution in presence of CHF, demyelination disorders. Increased risk of opportunistic infections.

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137 ■ Scalp: 10% salicylic acid in mineral oil qhs, tar shampoo qd, steroid lotion, calcipotriol lotion. ■ Nails: Intradermal triamcinolone acetonide injections (painful), methotrexate, new biologics. ■ Generalized psoriasis (⬎10% BSA) benefits from systemic therapy, best administered by an experienced physician.

Pyoderma Gangrenosum

Uncommon ulcerative skin condition with many potential associations. Etiology: ~50% are associated with systemic diseases, including: inflammatory bowel disease, polyarthritis, hematologic diseases/disorders (leukemia, myeloma, monoclonal gammopathies), hepatitis, Behçet syndrome. History: Acute onset with significant pain; arthralgias, malaise, mouth sores (aphthae), and/or abdominal pain may be present; lesions often occur after trauma to skin.

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N-S Physical: Initially superficial hemorrhagic pustule, then develops into painful boggy ulceration with dusky-violaceous undermined borders (#1 on lower leg), and heals with cribriform scars; can be single or multiple lesions. Several variants exist (ulcerative, bullous/atypical, pustular, & superficial granulomatous). Investigations: Biopsy is not specific and is mostly done to rule out other diagnoses. May swab for bacterial culture if signs and symptoms of infection. DDx: Antiphospholipid antibody syndrome, arterial insufficiency, traumatic ulceration, Sweet syndrome.

Management Investigate for and treat underlying diseases ■ Medical management: Surgery should be avoided. ■ Topical care: Appropriate dressings, topical or intralesional steroids or tacrolimus 0.1% ointment qd to immediate surrounding area. ■ Oral prednisone (1 mg/kg/d) initial therapy until healing begins; steroid-sparing agents: azathioprine, cyclosporine, mycophenolate mophetil, dapsone, infliximab ■ Other: Cyclosporine, cyclophosphamide, clofazimine, sulfapyridine, dapsone, minocycline.

Pyogenic Granuloma

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139 Common benign friable vascular growth (“proud flesh”). Etiology: Idiopathic or follows trauma to the skin; more common with oral retinoids & indinavir, and during pregnancy. History: Evolves quickly in children and young adults and bleeds easily; asymptomatic. Physical: Solitary, red, firm papule; often ulcerated and crusted; often on hands, fingers, face; may be sessile or pedunculated. Investigations: Clinical diagnosis; biopsy if uncertain. DDx: BCC, cherry angioma, Kaposi sarcoma, melanoma.

Management Remove offending drug if implicated; pregnancy-related lesions may self-resolve after delivery. Tx options: Excision, curettage & electrodessication, laser, liquid nitrogen cryotherapy.

Rosacea

Common chronic inflammatory disorder of pilosebaceous units and vasculature of the face. Role of Demodex mite controversial. History: Easy and recurrent flushing, exacerbated by heat (shower, hot drinks), spicy foods, sunlight, cold, alcohol, stress. Sensitive skin. May complain of dry and gritty eyes. Peak incidence 30—50 yr; F ⬎ M. Physical: Erythema, telangiectases, papules, and pustules of central face; no comedones in contrast to acne. Sebaceous hyperplasia, seborrheic dermatitis & facial lymphedema more common.

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N-S 4 Major Subtypes Erythematotelangiectatic, papulopustular, ocular, phymatous. ■ Chronic inflammation may progress to rhinophyma (enlarged nose; in males). Ocular involvement common (e.g., gritty, conjunctival injection, styes, photophobia). Investigations: Clinical diagnosis; uncommonly, skin biopsy to rule out lupus or sarcoidosis. DDx: Acne, lupus erythematosus, perioral dermatitis, sarcoidosis, seborrheic dermatitis.

Management ■ Based on severity and subtype. ■ Lifestyle modification: Avoid triggers; sun protection & avoidance; facial massage for lymphedema. ■ Topical antibiotics ■ Metronidazole 0.75% gel or 1% cream bid. ■ Sodium sulfacetamide lotion 10% bid. ■ Oral antibiotics (moderate to severe cases with inflammatory papulopustular component): ■ Tetracycline 500 mg po bid ■ Minocycline 100 mg po od—bid. ■ Doxycycline 20 mg po bid (subantimicrobial dose therapy) or 100 mg po qd–bid. ■ Isotretinoin (low dose); less commonly, topical retinoids may be used. ■ Laser therapy (e.g., PDL, IPL) for telangiectases & ablative laser (e.g., CO2) for rhinophyma. ■ Camouflage makeup (e.g., Dermablend™, Covermark®) for erythema. ■ Ophthalmologist to assess for ocular involvement (blepharitis, conjunctivitis, episcleritis).

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141 Sarcoidosis

Idiopathic condition characterized by noncaseating epithelioid granulomas affecting any organ system, most commonly the lungs. History: May have joint pain, fever, fatigue, weight loss, enlarged lymph nodes, anterior uveitis or other ocular findings. Lungs often affected, 1/3 symptomatically. Cutaneous involvement in 25%. Increased incidence in African Americans. Physical: Owing to potential multisystem involvement, clinical presentation is often variable. ■ Cutaneous lesions typically consist of oval red-purple-brown infiltrated plaques; tendency to infiltrate scars. Lupus pernio presents with violaceous indurated plaques on the face and is often associated with respiratory tract involvement. Erythema nodosum, a hypersensitivity reaction, may occur. Investigations: Biopsy needed to confirm diagnosis, with staining and cultures to R/O infectious causes of granuloma formation, e.g., mycobacterial and deep fungal infections; investigation for systemic involvement of sarcoidosis. DDx: Cutaneous tuberculosis, drug reaction, granuloma annulare or faciale, lichen planus, lupus.

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N-S

Management Localized cutaneous disease: Topical or intralesional corticosteroids Widespread systemic disease: Oral prednisone up to 1 mg/kg/d, hydroxychloroquine, steroid-sparing agents (e.g., methotrexate, azathioprine, cyclosporine), thalidomide.

Scabies

Courtesy of Dr. Loretta Fiorillo

Courtesy of Dr. Henry Foong Etiology: Parasitic infection by Sarcoptes scabiei var. hominis mite. History: Generalized and often debilitating pruritus, worse at night; family members or sexual partners may also itch. Usually transmitted by direct close human contact; incubation period 3—6 wk. More prone: Overcrowding & older patients in nursing homes, young children, & sexually active adults.

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143 Physical: Often nonspecific; papules & excoriations often present in the finger webs, flexor aspects of wrists, elbows, buttocks, genitalia (glans, nipples), with sparing of the head and neck. 4—8-mm linear ridges (burrow) with a gray dot at one end (mite) may be observed in the finger webs. Blisters may be noted (in infants). ■ Scabies often misdiagnosed as eczema; should be in differential diagnosis in the setting of persistent generalized pruritus. ■ Crusted “Norwegian” scabies: More extensive thick nodular infestation by numerous mites; observed in immunocompromised or neurologically impaired (e.g., Down syndrome) patients, & nursing homes. May not be pruritic. Investigations: If burrow is observed, scabies mites may be visible with a microscope upon examination of a scraping from a lesion prepared with mineral oil or KOH. Dermatoscope may also be helpful to visualize mite. DDx: Bug bites, eczema, lice, lichen planus, prurigo nodularis.

Management ■ Permethrin 5% cream (i.e., Nix®, Kwellada-P®) is the most reliable topical scabicide. ■ Patients should be instructed to apply cream to entire skin surface (neck down in adults, and entire body of infants and young children) with particular attention to finger-web spaces, feet, genitals, and intertriginous sites, and under nails; wash off in 8—14 hr (i.e., overnight application). ■ Despite 90% cure rate after a single treatment, repeat treatment 1 wk later; treatment resistance on the rise. ■ All household members and sexual partners should be treated simultaneously to prevent “ping-pong” re-infections. ■ All clothes worn within 2 d of treatment, towels, and bed sheets should be machine washed in hot water or dry cleaned. ■ Patients must be warned that pruritus may persist for weeks owing to delayed hypersensitivity response to the mite; treat with mid-potency steroids or oral prednisone course with taper and antihistamines prn. ■ Ivermectin po increasingly being used (esp. crusted scabies) owing to high efficacy, safety, & ease of use.

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Scars

Indurated and thickened, reddish plaque that forms at the site of the original injury and may be pruritic & tender. Unlikely to improve without treatment. ■ Most commonly found on the neck, shoulders, deltoid, and sternal region. ■ More common in Asians and blacks, & 10—30 yr. Hypertrophic scar remains confined to the site of injury and flattens in time and unlikely to be pruritic.

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145 Other Scars Acne scars: Due to prolonged duration of inflammatory papules, pustules, and nodules; major reason for treating acne early and aggressively. There are 5 types of acne scars: 1. Icepick scar: Jagged edge, steep sides, narrow, deep, extends into deep dermis or subcutaneous tissue 2. Boxcar scar: Round pits with sharp vertical edges 3. Rolling scar: Distensible, soft-shouldered, with rolling or undulating texture 4. Hypertrophic scar: Thick, raised, usually darker than surrounding skin 5. Train-track scar (shown): Criss-crossed scar resulting from wounds closed under tension and prolonged duration of sutures Investigations: Clinical diagnosis; biopsy if uncertain. DDx: None.

Management ■ Prevention is key; minimize surgeries in known keloid formers (ask people to tell or show you how they heal); minimize wound tension; avoid where possible surgery to prone areas & treat back and chest acne aggressively to avoid keloids. ■ Intralesional steroid injections with triamcinolone acetonide (Kenalog), 10mg—40 mg/ml, every 4—6 wk to flatten the scar and reduce pruritus. ■ Liquid nitrogen cryotherapy. ■ Laser therapy (CO2, PDL). ■ Occlusive dressings (e.g., silicone gel sheets) and mechanical compression (esp. earlobe keloids).

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N-S ■ Excision followed by intralesional steroids, topical imiquimod (Aldara®) 5% cream or radiation. ■ Acne scars: Dermabrasion or microdermabrasion, chemical peels, subcision, punch techniques, and augmentation with fillers. ■ “Train-track” scars: Surgical scar revision.

Sebaceous Hyperplasia

Common benign proliferation of sebaceous glands. History: Asymptomatic, very slow growing; more numerous in transplant pts. on cyclosporine. Physical: Single or multiple whitish-yellow small soft papules with central umbilication on face. Investigations: Clinical diagnosis; biopsy if uncertain (i.e., to R/O BCC). DDx: BCC, milia, molluscum contagiosum.

Management ■ Benign, treatment for cosmesis. ■ Liquid nitrogen cryotherapy, electrodesiccation & cautery, bichloroacetic acid, CO2 laser, photodynamic therapy, excision, isotretinoin.

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147 Seborrheic Dermatitis

Etiology: Common chronic inflammatory skin disease of sebumrich areas linked to Malassezia furfur, a commensal yeast. History: History of burning, itching, or scaling in typical distribution. More prevalent and severe in HIV and neurological diseases (e.g., Parkinson’s). Affects 3%—5% of population; two peaks, one in infancy and the other postpuberty; improves in summer. Physical: Excessive dandruff, orange-erythematous patches with loose dry or greasy scale; distributed in sebaceous gland regions—face (eyebrows, nasolabial folds, and retroauricular areas), scalp, chest, ears; infants: “cradle-cap.” Investigations: Clinical diagnosis; skin biopsy or fungal culture if uncertain. DDx: Contact or other forms of eczema, psoriasis, tinea.

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Management

Topical Antifungals

■ Nizoral shampoo (ketoconazole 2%), qd then taper with improvement. ■ Nizoral cream bid to body. ■ Oral antifungals in more resistant cases: ketoconazole 200 mg po qd x 10 d. ■ Mild topical steroids (often combined with topical antifungals) or steroid-sparing immunomodulators (tacrolimus or pimecrolimus). ■ Tar, zinc, sulfur, selenium sulfide, and salicylic acid shampoos regularly used & applied for 5—15 min prior to washing are beneficial for maintenance.

Seborrheic Keratosis (SK)

Common idiopathic benign epidermal growth in middle-age and elderly. History: Gradual development; occasionally pruritic or sore. Physical: Variably pigmented, waxy round-oval papules and plaques with verrucous or crusted surface, “stuck-on” appearance; most commonly: trunk, neck, arms, scalp; wide range of size.

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149 Leser-Trélat sign: Sudden, eruptive seborrheic keratoses in elderly individuals may be a sign of an associated internal (stomach cancer & others) malignancy; controversial. Investigations: Clinical diagnosis; skin biopsy if uncertain. DDx: AK, BCC, lentigo, nevus, melanoma, skin tag, wart.

Management ■ ■ ■ ■ ■ ■ ■

Treatment is for cosmesis or pruritus. Liquid nitrogen cryotherapy. ⫹/⫺ Curettage. Excision. Electrodesiccation. Laser (CO2). Topical tazarotene cream.

Skin Tag (Achrochordon)

Common benign fibrous growth of skin. History: Increase in size and number over time; usually asymptomatic, but may become bothersome and tender after trauma or torsion. More common in older people, females (especially during pregnancy), and the obese. Physical: Soft skin-colored to dark brown pedunculated polyp; commonly occur in axillae, neck, & groin. Investigations: Clinical diagnosis; shave/snip biopsy if uncertain. DDx: Nevus, SK, wart.

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Management ■ Benign and only require management if irritated or for cosmetic purposes. ■ Snipping with scissors (use local anesthesia if broad-based stalk). ■ Liquid nitrogen cryotherapy. ■ Electrodesiccation.

Squamous Cell Carcinoma (SCC)

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151 2nd most common form of skin cancer (after BCC) arising in sunexposed areas in elderly; due to malignant keratinocytes with metastatic potential. Etiology: Observed with: Chronic UV-damage, immunosuppression, burns, leg ulcers, chemical carcinogens (e.g., tar), HPV; can occur in discoid lupus, lichen sclerosus, & any scarring processes. History: Slow-growing, nonhealing scaly papule on sun-exposed area of head, neck, dorsal hands, and forearms; also affects mucous membranes (lower lip: M ⬎⬎ F, smokers, 10%—15% metastatic rate); rare in dark skin. Actinic keratosis is considered a precursor lesion; actinic cheilitis is the precursor on lip. Physical: Firm indurated papule, plaque, or nodule with adherent rough scale. Investigations: Biopsy (to mid-dermis) for confirmation. DDx: AK, BCC, SK, amelanotic melanoma, wart.

Management ■ ■ ■ ■

Electrodesiccation & curettage. Excision. Liquid nitrogen cryotherapy. Mohs micrographic surgery; less commonly topical imiquimod or radiation. ■ Advice on sun protection, regular skin exams.

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Stasis Dermatitis

Etiology: Common inflammatory skin condition of the legs usually associated with venous insufficiency due to varicose veins or other circulatory problems in middle-aged & elderly. History: Pruritus, leg edema, darkening color of legs. Physical: Erythema, scaling, eczema, commonly over the medial and anterior aspects of the shin and malleoli; edema & varicosities often noted; lichenification & hyperpigmentation develop in chronic cases. ■ Can be accompanied by a secondary autosensitization “id” dermatitis elsewhere on body (esp. if using prolonged topical antibiotics or anesthetics on legs). Investigations: Vascular studies prior to compression stockings if arterial disease suspected; skin biopsy if associated with chronic nonhealing ulcer. DDx: Cellulitis, contact dermatitis, pigmented purpuric dermatitis, pretibial myxedema.

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153 Management ■ Improve venous return by daily wear of compression support stockings (medical grade, fitted) & leg elevation; surgical intervention if not candidate or fails medical Tx. ■ Low-potency topical steroids and oral antihistamines prn. ■ Increased incidence of allergic reactions to ingredients in topical medicaments, hence avoid products containing lanolin, fragrances, bacitracin, neomycin, and other common sensitizers for prolonged periods of time.

Stevens-Johnson Syndrome (EM Major) and Toxic Epidermal Necrolysis (TEN)

Etiology: Spectrum of mucocutaneous drug-induced or idiopathic reaction pattern associated with impaired capacity to detoxify intermediate drug metabolites; genetic susceptibility; keratinocyte apoptosis (due to Fas & FasL interaction). History: Rare, high mortality rate (SJS, 5%; TEN, 30%) characterized by skin tenderness, erythema, desquamation, epidermal necrosis and sloughing affecting skin & mucous membranes, with systemic symptoms:

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N-S ■ SJS: lesions generally more macular, 2 mucous membranes involved and ⬍10% epidermal sloughing; typically drug started 1—3 wk prior to rash or feeling unwell with fever cough or sore throat (e.g., URTI with Mycoplasma). ■ TEN: Similar to SJS but ⬎ 30% of body surface area sloughed; stronger (95%) association with drugs as cause than SJS; typically drug started 1—3 wk prior to rash. Physical: Fever, stinging eyes, pain on swallowing, trunk lesions (dusky red macules that become gray in color) & flaccid blisters followed by spread; erosions & erythema of buccal, genital, & ocular mucosa in most cases. ■ Nikolsky sign: Rubbing unaffected skin induces lesion. ■ Common offending drugs: Anticonvulsants (esp. carbamazepine, phenytoin), NSAIDs, allopurinol, sulfa drugs; much higher incidence in HIV. Complications: Potentially life-threatening because of multisystem involvement, e.g., renal failure; severe ophthalmic involvement possible. Investigations: Skin biopsy; CBC&D, electrolytes, liver enzymes, Cr, urinalysis, INR, PTT, cultures of blood and denuded skin; CXR; consider bronchoscopy or upper GI series. DDx: Burn, bullous pemphigoid or lupus, linear IgA bullous disease, pemphigus—vulgaris or paraneoplastic.

Management ■ Requires Mx by experienced physician—usually dermatologist and/or plastic surgeon. ■ Can determine SCORTEN prognostic score (based on age, blood parameters, surface area, malignancy, & heart rate). ■ Remove & avoid offending drug (most important!). ■ Supportive care, often need ophthalmology assessment and ICU/burn unit admission. ■ Proper wound dressings, and antibiotics if any evidence of infection; antihistamines and topical steroids for pruritus; pain control and oral hygiene (e.g., Chlorhexidine rinse) important. ■ IVIG therapy is becoming standard of care; controversial.

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155 Striae (Stretch Marks, Striae Distensae)

Etiology: Progressive or rapid stretching of skin can lead to stretch marks, as with exercise, pregnancy (striae gravidarum), weight gain, rapid growth, anabolic steroids, Cushing’s disease. History: Occasionally pruritic. Hx of recent growth spurt, pregnancy, or steroid (topical, oral, anabolic) use. Physical: Initially pink hue and occasionally bright red-purple, eventually becoming thinned silvery-white depressed bands. Commonly on the abdomen, breasts, buttocks, lumbosacral, and thighs. Investigations: Clinical diagnosis; rarely need to R/O Cushing’s disease. DDx: Cushing’s disease, linear focal elastosis.

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Management Treatment is unsatisfactory. Wait & see: some improve with time, and pink-red color fades into silvery-white bands. Topical tretinoin (not during pregnancy) or laser therapy may potentially be effective.

Syphilis

Courtesy of Dr. William Gerstein

Courtesy of Dr. Henry Foong

Courtesy of Dr. Art Huntley

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157 Etiology: A chronic systemic disease due to Treponema pallidum spirochete transmitted sexually or through maternal-fetal route. History & Physical: It can affect multiple systems, with affinity for neural, cardiac, bone and cutaneous tissue, leading to widespread symptoms. ■ Three distinct phases: primary, secondary, then a period of latency (early, late) followed by tertiary phase. ■ 10: Painless chancre (usually genital) & enlarged regional lymph nodes, incubation period 10—90 d (avg ⫽ 3 wk) from inoculation, resolves spontaneously in a few weeks; asymptomatic infections common. ■ 20: 3—8 wk after primary infection, generalized nonpruritic red-brown macules and papules with palms and soles frequently involved, erosive patches in the mouth, condylomata lata (moist, pink nodules and plaques) on genital areas, “moth-eaten” alopecia; malaise, fever, & generalized lymphadenopathy; develops in all pts. in absence of Tx; resolves spontaneously within 3—8 wk; followed by a period of latency, may be life-long. ■ 30: 15%—40% of patients with untreated syphilis; multisystem disease which affects cardiac, nervous, and skeletal tissue as well as the skin: Ascending aortic aneurysms, CNS abnormalities, gummas (red-brown granulomatous plaques that erode into underlying cartilaginous and osseous tissue creating deformities). Rare. Investigations: Darkfield microscopy examination of serous fluid from 10 and most 20 lesions; presumptive diagnosis made via positive VDRL/RPR titer, but many false negatives and positives; FTA-ABS & TPPA treponemal assays are more specific for confirmation. DDx: Drug eruptions, erythema multiforme, herpes simplex, pityriasis rosacea.

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Management ■ Benzathine penicillin G 2.4 million units IM (in all stages of disease), schedule depends on stage. ■ Doxycycline, tetracycline, or erythromycin are second-line Tx choices (if penicillin allergic). ■ Patients should be tested for other STDs (esp. HIV).

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159 Tinea (Dermatophyte) Infections

Etiology: Dermatophytes digest and invade keratin and may infect skin, nails, and hair; incubation ⫽ 1—3 wk. Trichophyton, Microsporum, Epidermophyton species commonly involved. Human-to-human (anthropophilic), animal-to-human (zoophilic; intense inflammation), or soil-tohuman (geophilic; moderate inflammation) spread. Risk Factors: Hot, humid environments, sweating or maceration of the skin, occlusive footwear, diabetes mellitus, immunosuppression (e.g., AIDS). History: Asymptomatic; occasionally mild pruritus. Physical: Scalp hair and general body surfaces mostly affected during childhood; hand, foot, or nail infections are more common after puberty. ■ Immunologic response to a dermatophyte infection may result in a dermatophytid or “id” reaction: Vesicular eruption on acral surfaces, especially the palms. Investigations: Skin scraping analysis with KOH prep—Septate hyphae branching at various angles are seen; fungal culture (~4 wk to ID dermatophyte species); biopsy—PAS or GMS stain can reveal presence of fungal elements. DDx: Eczema, granuloma annulare, psoriasis. )

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Tinea Corporis Affects trunk and extremities: Erythematous annular scaly patches with “active border,” central clearing; #1 cause ⫽ T. rubrum.

Tinea Pedis

1. Interdigital type: Macerated, scaly plaques in toe web spaces, can be portal of entry for cellulitis of the foot, especially in diabetics. (Tip: in recurrent leg cellulitis, look for tinea pedis!) 2. “Moccasin” type: Dryness, scaling and erythema of the plantar and/or lateral foot.

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161 3. Vesicular type: vesicles, pustules, or bullae on the feet. ■ “One hand, two feet disease”: Common clinical presentation of tinea pedis involving one hand and both feet.

Tinea Cruris

Inner thighs and inguinal folds; tinea faciei: face; tinea manuum: hands; tinea barbae: beard area.

Tinea Capitis Alopecia with scale, kerion (boggy mass), or discrete pustules; very contagious.

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Tinea Unguium/Onychomycosis See onychomycosis section.

Management Patient education: Avoid factors which predispose to infection, absorbent powders in intertriginous areas, e.g., for tinea pedis— shower-shoes in public facilities. Topical antifungals for tinea corporis/cruris/pedis (unless lesions are extensive): Terbinafine, ciclopirox, clotrimazole, ketoconazole applied qd or bid x 3 wk, or continue 1 wk until after resolution of lesions. Systemic antifungals for tinea capitis. 1. Terbinafine (Lamisil) ⬍20 kg ⫽ 62.5 mg po qd, 20—40 kg ⫽ 125 mg po qd, ⬎40 mg ⫽ 250 mg po qd x 2—4 wk. 2. Micronized griseofulvin with food: 20 mg/kg/d po x 8 wk; adults: 500 mg po qd x 1 mo. 3. Patient and household contacts should use an antifungal shampoo, such as selenium sulfide or ketoconazole to reduce spread.

Ulcers, Leg

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163 Etiology: Most common lower extremity ulcers are: venous, arterial or neuropathic; can be mixed. Other causes: Trauma (⫹ above), vasculitis, pyoderma gangrenosum, bacterial infections, malignancy, vasospastic (e.g., cryoglobulinemia, sickle cell anemia).

Ulcer Type Venous (mostcommon; 70%)

Arterial

Neuropathic

Clinical

Management

Occur in malleolar region; Compression irregular borders; stasis wraps and, once changes, edema, varicose healed, support veins, hemosiderosis, stockings for life. painful. Occur in pressure sites & If possible, surgery toes; necrotic base, to restore punched out w/ shiny arterial blood atrophic surrounding flow. skin; history of claudication, decreased/ absent pulses & prolonged capillary refill. Occur over pressure areas; Relieve (off-load) punched out w/ surpressure by rounding callus; special shoes, decreased sensation; casts or most commonly assocrutches, better ciated with diabetes. diabetes control.

History: Ask about—onset & course, symptoms, PMHx, social history, & meds. Major morbidity and financial cost. Physical: Inspect & document—location, size, shape, odor, ulcer edge & base features, surrounding skin (cellulitis, dermatitis), peripheral pulses, & capillary refill. Investigations: Vascular studies, blood tests, culture & biopsy wound edge; bone scan if you suspect chronic process or osteomyelitis. DDx: Pyoderma gangrenosum, vasculitis, SCC.

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Management

Principles of Wound Care Treat any underlying cause: ■ Venous insufficiency—compression. ■ Arterial insufficiency—surgery. ■ Neuropathic or decubitus ulcer—pressure relief. ■ Infection—antibiotics. ■ Neoplasm—surgery, radiation. ■ Promote wound healing. ■ Débride: Enzymes, surgery/curette. Dressings: Promote moisture, but not oozing/weeping; know your dressings— foams, alginates, hydrogels, hydrocolloids, hydrofibers. ■ Infection control: Topical or oral Abx. ■ Skin grafting. ■ Less commonly: skin substitutes, growth factors. Allergic contact dermatitis common with long-term topical antibiotic use (esp. bacitracin, neomycin); use petroleum jelly— low allergenicity, safe, & cheap. Compression stockings required if evidence of pitting/stasis dermatitis; obtain ankle-brachial index prior to initiating treatment; medical grade better than over-the-counter. Topical metronidazole eliminates odor. Short-contact topical tretinoin appears to be beneficial. Biopsy ulcer if fails to improve with care.

Ulcers, Pressure (Decubitus)

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165 Etiology: The trigger event is compression of the tissues against an external object: e.g., mattress, wheelchair, or bed rail. Persistent (i.e., ⬎ 2 hr) pressure in excess of capillary filling pressure (32—35 mm Hg) leads to tissue ischemia, necrosis, and ulceration. Shear forces and friction aggravate the effects of pressure. History: Immobility is the key risk factor, with the elderly and neurologically impaired most prone. High morbidity and mortality, particularly because of superinfection of pressure ulcers. Physical:

Pressure Ulcer Staging Stage 1 Stage 2 Stage 3

Stage 4

Nonblanchable erythema of intact skin Partial-thickness skin loss involving the epidermis and/or dermis Full-thickness skin loss with damage to the subcutaneous tissue that may extend down to, but not through, the underlying fascia Full-thickness skin loss with extensive destruction, tissue necrosis, or damage to muscle, bone, or supporting structures.

Investigations: Culture to identify and quantify bacterial colonization; biopsy in persistent nonhealing ulcers. DDx: SCC, pyoderma gangrenosum, osteomyelitis.

Management Prevention is paramount: Turn and reposition the patient often (e.g., q 2 hr). Specialized pressure-diffusing beds and support cushions. Surrounding intact skin must be kept clean and dry. Assess and treat bacterial infection. Débridement (chemical, physical) of necrotic tissue. Adequate nutrition necessary for good wound healing. Consider Wound Vac®. Multidisciplinary approach is best.

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Urticaria (Hives)

Etiology: Common vascular reaction pattern of the skin. Histamine release from mast cells in the dermis from immunologic or nonimmunologic mechanisms. Causes of acute urticaria: Foods: Fish, shellfish, eggs, nuts, strawberries. Infections #2: viral (e.g., URTI), bacterial (e.g., strep throat, sinusitis, UTI), parasitic. Drugs: Aspirin, NSAIDs, alcohol, codeine, morphine, penicillin, sulfonamides, thiazides. Insect stings. Systemic illness—i.e., lupus, malignancies. Idiopathic—#1 History: Transient migratory wheals, individual lesions last ⬍24 hr, marked pruritus; up to 15% lifetime incidence; F ⬎ M. May be acute ⬍6 wk or chronic ⬎6 wk. Special forms of urticaria: cholinergic, contact, physical (aquagenic, adrenergic, cold, dermatographism, heat, pressure, solar, vibratory), urticarial vasculitis (wheals last ⬎24 hr), C1 esterase inhibitor deficiency (rare). Physical: Annular or arciform erythematous, edematous papules and plaques; may become confluent to form serpiginous or polycyclic patterns.

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167 Investigations: Often not warranted in acute urticaria; order tests to confirm suspected causes, e.g., CBC, ESR, C4, TSH, ASOT titers, sinus films, U/A, stool for O&P; skin biopsy if lesions persist ⬎24 hr; consider work-up if chronic. DDx: Insect bites, urticarial bullous pemphigoid, mastocytosis, erythema multiforme, urticarial vasculitis, angioedema.

Management ■ Ask about facial edema or difficulty breathing, which may be warning signs of systemic anaphylaxis. ■ Identify and eliminate etiologic agents. ■ Avoid aggravating factors: ACE-I, ASA, codeine, morphine, NSAIDs. ■ Minimize: Stress, heat, alcohol. Symptomatic relief: Mild cases: Low sedating H1 blockers Zyrtec (cetirizine) 10 mg po qd, Allegra (fexofenadine) 60 mg po bid or Claritin (loratidine) 10 mg po qd or Aerius/Clarinex (desloratidine) 5 mg po qd. Moderate cases: Doxepin 25 mg po qHS. Severe cases: Prednisone taper x 3 wk for symptomatic relief (avoid in chronic cases); other: cyclosporine, plasmapheresis, IVIG Epipen on discharge, if severe reaction.

Vasculitis, Leukocytoclastic

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T-Z Etiology: Often a reaction pattern to internal or external agent; broadly divided into categories: infections, drugs, malignancy, autoimmune connective tissue disease, idiopathic. History: Symptoms include itching, burning, or pain. Can also be asymptomatic. May have internal involvement and symptoms, e.g., fever, arthritis, abdominal pain, diarrhea, cough, weakness, sinusitis, & hematuria. Physical: Palpable purpura, most commonly over lower legs (dependent areas). Investigations: Work-up for potential trigger and assessment of systemic involvement, esp. renal; CBC&D, liver enzymes, urinalysis, CRP, Hep B & C, cryoglobulins, ANA, ENA, ANCA, RF, complement; skin biopsy (reveals small vessel vasculitis); immunofluorescence to rule out HSP. DDx: Thrombocytopenia or ITP or TTP, meningococcemia, other vasculitic syndromes.

Management Supportive care and treatment of underlying cause (e.g., infections—Hep C). Removal of causative agent (e.g., drugs—especially antibiotics, allopurinol, thiazides). Therapy depends on whether there is evidence of internal vasculitis. Oral prednisone, colchicine, dapsone, steroid-sparing immunosuppressive agents (e.g., azathioprine).

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169 Vitiligo

Acquired skin disorder characterized by well-defined areas of complete epidermal depigmentation; various pathogenesis theories; likely a large autoimmune component. History: Asymptomatic; 50% present before age 20; 1%—2% affected; rare in infancy & old age. ■ Associated with immune disorders; therefore work-up for thyroid disease (TSH), diabetes, pernicious anemia, and other autoimmune diseases occasionally indicated (e.g., family history). Physical: Stark white patches with well-demarcated border; hair in vitiligo patches appears white or gray; several variants: segmental, acrofacial, mucosal, etc. Course: increased risk of sunburn and skin cancer in amelanotic areas; frustrating to Tx.

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T-Z Investigations: Wood’s lamp accentuates areas of vitiligo & helps determine extent; skin biopsy uncommonly; consider TSH and fasting blood glucose. DDx: Leprosy, pityriasis alba, tinea versicolor, tuberous sclerosis, nevus anemicus, or depigmentosus.

Management ■ Mainly for cosmetic/psychological burden; consider assessment for diabetes, thyroid & Addison disease. ■ Topical steroids and new topical immunomodulators (tacrolimus & pimecrolimus), PUVA, NB-UVB phototherapy, camouflage makeup; oral steroid rarely used. ■ Note that facial and more proximal lesions respond better than acral lesions. ■ Surgical transplants can be considered in stable vitiligo— uncommon ■ If extensive, rarely can consider bleaching of nonaffected areas to result in total white color. ■ Advise re: importance of sun protection. ■ Autologous transplantation or grafting of cultured autologous melanocytes in stable vitiligo (still in research); 308-nm excimer laser (being studied).

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171 Warts (Verrucae)

Etiology: Cutaneous intraepidermal viral infection caused by different subtypes of human papilloma virus (HPV) transmitted directly through broken skin. History: Affects up to 20% of school-aged children; more common in immunosuppressed and transplant patients; occasionally painful (plantar); can cause psychosocial distress. Types: Vulgaris (common warts), plantar, flat, genital (condyloma acuminata).

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T-Z Physical: Flesh-colored hyperkeratotic firm papules, disrupt normal fingerprint lines and display small black dots (thrombosed capillaries). Course: Genital HPV types 16, 18, and 31 can act to promote development of SCC. DDx: Molluscum contagiosum, SK, SCC.

Management ■ Conservative: Wait & see, 20%—30% clear w/i 6 mo, 50% w/i 1 yr, & 66% w/i 2 yr. ■ Patient counseling if anogenital warts to reduce transmission (e.g., condoms) and tests for other STDs. Also at higher risk for anogenital malignancies—females should have annual PAP smears. ■ The goal of therapy is superficial destruction of affected skin and elicitation of immune response. ■ Plantar warts are thick and should be pared down; can soak foot in water to ease paring. ■ Liquid nitrogen—swab or cryospray (avoid in pts. with dark skin), repeat every 3—4 wk. ■ Podophyllin 25% for genital warts x 4—6 hr (avoid contact with normal skin) and washed at home; repeat weekly. ■ Salicylic acid (up to 40%) OTC—home treatment. ■ Duct tape—may be useful in plantar warts, leave on for 1 wk then replace. ■ Electrodesiccation ⫹/- curettage. ■ Trichloroacetic acid (80%—90%). ■ Immunotherapy with diphencyprone (DPC). ■ Intralesional bleomycin, candidal antigen for resistant warts. ■ Topical retinoids (esp. flat warts). ■ Imiquimod 5% cream (esp. genital warts) or topical 5-FU. ■ Scissors excision. ■ CO2, PDL laser vaporization. ■ In case of extensive perivaginal or perianal warts, referral to gynecologist or gastroenterologist, respectively, to assess internal involvement. ■ Vaccines currently in development (for HPV 6,11,16,18).

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173 Acronyms & Abbreviations Abx ACD ACE-I AK ANCA ANA ASA BCC BID BP BSA BUN Bx CBC (&D) CF CHF CHILD syndrome CK Cr CREST

CRP C&S CTCL DEJ DF DHEA(S) DIF DLE EM ENA ESR F FSH 5-FU

Antibiotics Allergic contact dermatitis Angiotensin converting enzyme inhibitor Actinic keratosis Antineutrophil cytoplasmic antibodies Antinuclear antibody Acetyl salicylic acid (aspirin) Basal cell carcinoma Bis in die (twice a day) Bullous pemphigoid Body surface area Blood urea nitrogen Biopsy Complete blood count (& differential) Cystic fibrosis Congestive heart failure Congenital hemidysplasia, ichthyosiform erythroderma, and limb defects Creatine kinase Creatinine Calcinosis cutis, Raynaud’s phenomenon, esophageal dysfunction, sclerodactyly, telangiectasia C-reactive protein Culture & sensitivity Cutaneous T-cell lymphoma Dermal-epidermal junction Dermatofibroma Dehydroepiandrosterone (sulfate) Direct immunofluorescence Discoid lupus erythematosus Electron microscopy Extractable nuclear antigen Erythrocyte sedimentation rate Female Follicle-stimulating hormone 5-Fluorouracil

TOOLS

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TOOLS GVHD Hgb H&E HPV HSP IBD ICAM IIF ILVEN IM ITP IV IVIG KA KOH KP LCV LH LP LS & A M MCV MF MM MTX Mx NF NSAIDs OD OTC PCOS PCR PCT PHN PMHx PPD PPD PRP

Graft-versus-host disease Hemoglobin Hematoxylin & eosin Human papillomavirus Henoch-Schönlein purpura Inflammatory bowel disease Intracellular adhesion molecule Indirect immunofluorescence Inflammatory linear verrucous epidermal nevus Intramuscular Idiopathic thrombocytopenic purpura Intravenous Intravenous immunoglobulin Keratoacanthoma Potassium hydroxide Keratosis pilaris Leukocytoclastic vasculitis Luteinizing hormone Lichen planus Lichen sclerosus et atrophicus Male Molluscum contagiosum virus Mycosis fungoides Malignant melanoma Methotrexate Management Neurofibromatosis Nonsteroidal anti-inflammatory drugs Once a day Over the counter Polycystic ovarian syndrome Polymerase chain reaction Porphyria cutanea tarda Postherpetic neuralgia Past medical history Paraphenylenediamine Purified protein derivative (TB skin test) Pityriasis rubra pilaris

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175 PUPPP R/O SC SCC SJS SK SLE STDs TBSE TEN TPPA TTP Tx Ungt URTI U/S UV(L) VZV yo

Pruritic urticarial papules & plaques of pregnancy Rule out Subcutaneous Squamous cell carcinoma Stevens-Johnson syndrome Seborrheic keratosis Systemic lupus erythematosus Sexually transmitted diseases Total body skin examination Toxic epidermal necrolysis Treponema pallidum particle agglutination test Thrombotic thrombocytopenic purpura Treatment Ointment Upper respiratory tract infection Ultrasound Ultraviolet (light) Varicella zoster virus Years old

Spanish-English Vocabulary & Translation Abscess Acne Allergic dermatitis Allergies Allergy Address Adverse effect Antiallergenic Antibiotic Antifungal

El absceso El acné La dermatitis alérgica Las alergias La alergia La dirección La reacción adversa, el acontecimiento adverso (for FDA and IRBs) El antialérgico El antibiótico El antimicótico, para la infección por hongos (Continued text on following page)

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Spanish-English Vocabulary & Translation (Cont’d) Antihelminthic Antihistamine Arthralgia, joint pain

Bacterial infection Bandage BID (twice a day) Birth mark Bite Biopsy Blister Blistering disease Blood chemistry Blood culture Blood work Body hair Boils Bruising Burn Candida/yeast infection Cash Canker sores Chickenpox Condom Contraceptive Contraceptive pill

Medicamento para las lombrices Los antihistamínicos El dolor en las articulaciones, dolor en las coyunturas, el cuerpo “cortado,” la artralgia La infección bacteriana/infección bacterial La venda, el vendaje, el apósito Bid, dv/d La mancha de nacimiento La mordida, mordedura La biopsia La ampolla La enfermedad ampollosa La química sanguínea El hemocultivo El análisis de sangre El vello Los forúnculos Los moretones, cardenales La quemadura La candidosis/la candidiasis El efectivo El afta/la estomatitis aftosa La varicella El preservativo/condón El anticonceptivo La píldora anticonceptiva (Continued text on following page)

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177 Spanish-English Vocabulary & Translation (Cont’d) Contraindications Co-pay Cosmetics Cream Credit card Cyst Dandruff Dermatitis Dermatologist Dermatology Diaphragm Difficult to treat Diarrhea Dosage Dose Drug Drug (illicit, recreational) Drug eruption

Drug reaction

Dry mouth Dry skin Drug interactions

Las contraindicaciones El pago compartido, copago Los cosméticos La crema La tarjeta de crédito El quiste La caspa La dermatitis, ronchas El dermatólogo (la dermatóloga) La dermatología El diafragma Difícil de tratar La diarrea La dosificación La dosis El medicamento, fármaco, la medicina La droga La erupción provocada por un medicamento/fármaco—la erupción yatrógena/la erupción medicamentosa/el exantema medicamentoso La reacción a un medicamento/ fármaco—la reacción yatrógena/ la reacción medicamentosa La boca reseca La piel reseca Las interacciones farmacológicas (Continued text on following page)

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Spanish-English Vocabulary & Translation (Cont’d) Eczema Family physician Father Fatigue Fever Fill-out Folliculitis Form Full name Fungus infection Gauze Gel Generic drug Genital area Genitals Hair Hair loss Harmless growth Hives/urticaria Hospital Hyperpigmentation Hypertrichosis Hypopigmentation Immune globulin Impetigo

El eczema El médico familiar El padre El agotamiento, la fatiga La fiebre, calentura Llenar, completar La foliculitis El formulario, la forma (México) El nombre completo La infección micótica, la infección por hongos La gasa El gel Los medicamentos genéricos El área genital Los genitales El pelo/el cabello La alopecía/la pérdida del cabello/ la caída del cabello La masa benigna/el tumor benigno/ la neoplasia benigna Las ronchas/la urticaria El hospital, la clínica, el sanatorio La hiperpigmentación La hipertricosis/el hirsutismo La hipopigmentación La inmunoglobulina El impétigo (Continued text on following page)

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179 Spanish-English Vocabulary & Translation (Cont’d) Inherited skin disease

Insect bite Intravenous (i.v.) Interpreter Irritant dermatitis IUD Keloid Laser(s) Leprosy Lice Lotion Lupus (erythematosus) Lymph nodes Malaise Married Measles Medical (adj) Medical history Medical insurance Melanoma Mole Mother

Myalgia

La enfermedad hereditaria de la piel/ la dermatosis hereditaria/ la dermatopatía hereditaria El piquete de insecto Intravenoso(a), endovenoso(a) El intérprete (la intérprete) La dermatitis irritativa El dispositivo intrauterino/el “aparato” La cicatriz queloide/el queloide El láser/los láser La lepra Los piojos La loción El lupus/el lupus eritematoso Los ganglios linfáticos El malestar Casado El sarampión Médico, médica Los antecedentes médicos, el historial médico, la historia médica Seguro médico El melanoma El lunar Madre (su señora madre, su mamá, mi mamá, mi madre. Do not use “su madre.”) Los dolores musculares, mialgia (Continued text on following page)

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Spanish-English Vocabulary & Translation (Cont’d) Nails Nausea NSAIDs Nurse (n) Occupation Office (medical) Office hours Ointment Old age spot (harmless) Orally Oral medication Over-the-counter medications Pain medication Patient Perfume Pharmacy Pill, the Please take a seat Precancer Pregnancy test Prescription drugs

PRN (as needed)

Las uñas Las náuseas, la náusea Los medicamentos antiinflamatorios no esteroides La enfermera (el enfermero) Ocupación, empleo, trabajo El consultorio Horas hábiles Ungüento Las manchas de la vejez Por vía oral El medicamento oral Los medicamentos de venta libre; medicamentos que no requieren receta médica Los medicamentos para el dolor, los analgésicos El paciente (la paciente) El perfume, el agua de colonia La farmacia, la botica, el dispensario médico (small towns) La píldora/la pastilla Por favor tome asiento; tenga a bien tomar asiento Precáncer La prueba de embarazo Los medicamentos de venta controlada; medicamentos que requieren receta médica PRN (según se requiera) (Continued text on following page)

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181 Spanish-English Vocabulary & Translation (Cont’d) Problem Pruritus Psoriasis Pus QD (every day) QD (every day) Rash Receptionist Redness Referring physician Relatives Resident Results Rheumatoid arthritis Rosacea Roseola Salve Scar Scabies Scalp Sexually transmitted disease Shampoo Skin cancer Skin rash Skin tag

El problema La comezón, el prurito La psoriasis El pus Diario Todos los días La erupción de la piel, la urticaria La recepcionista El enrojecimiento El médico remitente Los parientes El residente (la residente) Los resultados La artritis reumatoide La rosácea La roséola El bálsamo, la pomada La cicatriz La sarna El cuero cabelludo Las ETS/las enfermedades de transmisión sexual/las enfermedades venéreas El champú El cáncer de la piel El exantema/la erupción cutánea La turgencia cutánea/el acrocordón/ el papiloma cutáneo (Continued text on following page)

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Spanish-English Vocabulary & Translation (Cont’d) Sore Sores Steroids Strep throat Subcutaneous Surgeon Surgery Swelling Symptom Syphilis Tablespoon Tablet Teaspoon Tenderness Thrush TID (three times a day) Toilet/commode Topical Topical medication Ulcer Viral infection Vitiligo Vomiting Warts Wife

La llaga/la úlcera Las lesiones, las úlceras Los esteroides La infección de la garganta por estreptococos Subcutáneo(a) El cirujano (la cirujana) La cirugía La hinchazón El síntoma La sífilis La cucharada El comprimido, la tableta, la pastilla La cucharadita Un poco de dolor El algodoncillo tid, tv/d (tres veces al día) El inodoro, la taza, el water, el WC (escusado, slang) Tópico(a) El medicamento tópico La úlcera La infección vírica/infección viral El vitíligo/la leucodermia adquirida El vómito Las verrugas La esposa

Courtesy of Verónica Albin.

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183 Synonyms Index Medical Terminology Acrochordon Actinic keratosis Actinic purpura Androgenetic alopecia Aphthous ulcers Asteatotic eczema/ dermatitis Atopic dermatitis Bloom syndrome Bowen disease Buerger syndrome Buschke-Ollendorf syndrome Campbell de Morgan spot Candidiasis Churg-Strauss syndrome Clark nevus Coccidiomycosis Condylomata acuminata Crowe sign Cutaneous larva migrans Cutaneous T-cell lymphoma Darier disease Decubitus ulcer Degos disease Dermatoheliosis

Synonyms and Layman’s Terms Skin tag Solar keratosis Solar or senile purpura Male-pattern baldness Canker sores Eczema craquelé Atopic eczema; eczema Congenital telangiectatic erythema Squamous cell carcinoma in-situ Thromboangiitis obliterans Dermatofibrosis lenticularis Cherry (hem)angioma Moniliasis Allergic granulomatosis Dysplastic nevus San Joaquin Valley fever Genital warts Axillary freckling Creeping eruption Mycosis fungoides Keratosis follicularis Pressure ulcer Malignant atrophic papulosis Photoaging (Continued text on following page)

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Synonyms Index (Continued) Medical Terminology Digital mucous cyst Discoid lupus erythematosus Dyshidrotic eczema Eczema herpeticum Ephelides Epidermoid cyst Epidermolytic hyperkeratosis Erythema induratum (of Bazin) Erythema infectiosum Fabry syndrome Favre-Racouchot syndrome Fish tank granuloma Fox-Fordyce disease Furunculosis Geographic tongue Gianotti-Crosti syndrome Glomus tumor Glossodynia Goltz syndrome Gorlin syndrome Gougerot-Carteaud papillomatosis/syndrome

Synonyms and Layman’s Terms Digital myxoid cyst; synovial cyst Chronic cutaneous lupus erythematosus Pompholyx Kaposi’s varicelliform eruption Freckles Sebaceous cyst; wen; epidermal cyst Bullous congenital ichthyosiform erythroderma Nodular vasculitis Fifth disease Angiokeratoma corporis diffusum Nodular elastosis with cysts and comedones Mycobacterium marinum infection Apocrine miliaria Boils Migratory glossitis Papular acrodermatitis of childhood Glomangioma Burning mouth syndrome Focal dermal hypoplasia Nevoid basal cell carcinoma syndrome; basal cell nevus syndrome Confluent and reticulated papillomatosis (Continued text on following page)

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185 Synonyms Index (Continued) Medical Terminology Granuloma inguinale

Grover disease Günther disease Hailey-Hailey disease Hansen disease Hemangioma of infancy Herpes labialis Herpes zoster Hutchinson freckle Hyperhidrosis Job syndrome Kawasaki syndrome Koilonychia Kyrle disease

Synonyms and Layman’s Terms Donovanosis Transient acantholytic dermatosis Erythropoietic porphyria Benign familial pemphigus Leprosy Strawberry hemangioma; infantile hemangioma Cold sore; fever blister Shingles Lentigo maligna Excess sweating Hyper IgE syndrome Mucocutaneous lymph node syndrome Spoon nails Hyperkeratosis follicularis et parafollicularis in cutem penetrans Hypersensitivity vasculitis Lichen sclerosus et atrophicus Rubeola Chloasma Cheilitis granulomatosa

Leukocytoclastic vasculitis Lichen sclerosus Measles Melasma Melkersson-Rosenthal syndrome Miliaria rubra Prickly heat Morphea Localized scleroderma Mucha-Habermann Pityriasis lichenoides et varioliformis diseaseSynonyms Index acuta (PLEVA)


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Synonyms Index (Continued) Medical Terminology

Synonyms and Layman’s Terms

Mucocele Mycetoma Mycosis fungoides Myxoid cyst Nevus or nevi Nevus sebaceus Norwegian scabies Nummular eczema Ofuji’s disease Onychomycosis Osler-Weber-Rendu disease Papular urticaria Pediculosis Pediculosis pubis Pemphigoid gestationis Pilomatricoma Pityriasis versicolor Port-wine stain Pseudofolliculitis barbae PUPPP

Ranula Madura foot Cutaneous T-cell lymphoma Digital mucous cyst Mole(s) Organoid nevus Crusted scabies Discoid eczema Eosinophilic folliculitis Tinea unguium Hereditary hemorrhagic telangiectasia (arthropod) bite reaction Lice Crab lice; pubic lice Herpes gestationis Calcifying epithelioma of Malherbe Tinea versicolor Nevus flammeus Beard bumps (Pruritic urticarial papules & plaques of pregnancy) Polymorphic eruption of pregnancy (PEP) Lobular capillary hemangioma Reactive arthritis Exanthem subitum; sixth disease Poikiloderma congenita

Pyogenic granuloma Reiter syndrome Roseola infantum Rothmund-Thomson syndrome


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187 Synonyms Index (Continued) Medical Terminology Rubella Schamberg disease Scleroderma Seborrheic dermatitis Sneddon-Wilkinson disease Spider angioma Spitz nevus Stein-Leventhal syndrome Striae Sweet syndrome Syphilis Temporal arteritis Tinea corporis Tinea cruris Tinea pedis Trichilemmal cyst Ulerythema ophryogenes Urticaria Varicella Verruca vulgaris Von Recklinghausen disease Wells’ syndrome Werner syndrome Woringer-Kolopp disease Xerosis Zoon balanitis

Synonyms and Layman’s Terms German measles Progressive pigmentary purpura Progressive systemic sclerosis “Cradle cap” (infants); dandruff Subcorneal pustular dermatosis Spider nevus; nevus araneus Juvenile melanoma Polycystic ovary syndrome Stretch marks Acute febrile neutrophilic dermatosis Lues Giant cell arteritis Ringworm Jock itch Athlete’s foot Pilar cyst; wen Keratosis pilaris atrophicans faciei Hives Chickenpox Wart (common) Neurofibromatosis type I Eosinophilic cellulitis Progeria Pagetoid reticulosis Dry skin Balanitis circumscripta plasmocellularis

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Websites of Interest For Healthcare Workers American Academy of Dermatology (AAD): http://www.aad.org Dermanities: http://www.dermanities.com Dermatology Information System (DermIS): http://dermis. multimedica.de Dermatology Nurses Association (DNA): http://dna.inurse.com Dermatology Physician Assistants: http://home.pacifier.com/ ~jomonroe Dermatology Times: http://www.dermatologytimes.com/ dermatologytimes DermMD: www.gizmodoc.com/dermmd Electronic Textbook of Dermatology: http://www.teleme dicine.org/stamford.htm E-medicine dermatology: www.emedicine.com/derm/index.shtml Evidence-Based Dermatology portal: http://www.ebderm.org Medical Student Core Curriculum from the AAD: http://www.aad. org/professionals/Residents/MedStudCoreCurr

For Patients Alliance for Humane Dermatology: http://www.ahd.ca DermNet: http://www.dermnetnz.org/index.html Healthfinder: http://www.healthfinder.gov Quackwatch: http://www.quackwatch.org Skin Care Physicians: http://www.skincarephysicians.com

Support Groups American Autoimmune Related Diseases Association: http://www.aarda.org American Behcet’s Disease Association: http://www.behcets.com American Hair Loss Council: http://www.ahlc.org American Porphyria Foundation: http://www.porphyria foundation.com Ataxia-Telangiectasia Children’s Project: http://www.atcp.org Camp Discovery: http://www.aad.org/public/Parentskids/ CampDisIntro.htm Congenital Nevus Support Group: http://www.nevusnetwork.org

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189 Dystrophic Epidermolysis Bullosa Research Association of America (DebRA): http://www.debra.org Ehlers-Danlos National Foundation: http://www.ednf.org Foundation for Ichthyosis & Related Skin Types (FIRST): http:// www.scalyskin.org Genetic Alliance: http://www.geneticalliance.org Gluten Intolerance Group of North America—Dermatitis Herpetiformis: http://www.gluten.net Hereditary Hemorrhagic Telangiectasia Foundation: http://www.hht.org Histiocytosis Association of America: http://www.histio.org International Forum for the Study of Itch & Living with Itch: http://www.itchforum.org International Pemphigus Foundation: http://www.pemphigus.org Leukemia & Lymphoma Society: http://www.leukemia.org Lupus Foundation of America: http://www.lupus.org Med Help: http://www.medhelp.org Mycosis Fungoides Foundation (MFF): http://www.mffoundation. org National Alopecia Areata Foundation: http://www.naaf.org National Association for Pseudoxanthoma Elasticum: http:// www.pxenape.org National Eczema Association for Science & Education (NEASE): http://www.nationaleczema.org National Foundation for Ectodermal Dysplasias: http://www.nfed. org National Institutes of Health: http://www.nih.gov National Organization for Albinism and Hypopigmentation (NOAH): http://www.albinism.org National Organization for Rare Disorders: http://www. rarediseases.org National Psoriasis Foundation: http://www.psoriasis.org National Rosacea Society: http://www.rosacea.org National Vitiligo Foundation: http://www.vitiligofoundation.org Nevus Outreach: http://www.nevus.org Pityriasis Rubra Pilaris Support Group: http://prp-support.org Proteus Syndrome Foundation: http://www.proteussyndrome.org

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TOOLS Pseudoxanthoma Elasticum, Inc.: http://www.pxe.org Scleroderma Foundation: http://www.scleroderma.org Scleroderma Research Foundation: http://www.srfcure.org Sjögren’s Syndrome Foundation: http://www.sjogrens.com Skin Cancer Foundation: http://www.skincancer.org Sturge-Weber Foundation: http://www.sturge-weber.com Tuberous Sclerosis Alliance: http://www.tsalliance.org Vascular Birthmarks Foundation: http://www.birthmark.org Xeroderma Pigmentosa Society: http://www.xps.org

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191 Additional Skin Diseases & Disorders

Amyloidosis

Angiofibroma

Atrophie blanche

Becker nevus

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Additional Skin Diseases & Disorders (Cont’d)

Burn (oven)

Callus

Cuti rhomboidalis nuchae

Dermatoheliosis

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193 Additional Skin Diseases & Disorders (Cont’d)

Dyshidrotic eczema

Elephantiasis nostra verrucosum

Erosio interdigitalis blastomycetica

Fixed drug eruption

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Graft versus Host Disease

Hailey-Hailey Disease

Halo Nevus

Juvenile xanthogranulomas

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Koebnerization – in psoriasis

Leprosy – tuberculoid

Leichmaniasis

Lichen amyloidosis

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Linear epidermal nevus

Lipodermatosclerosis

Palmoplanter Keratoderma

Periungal fibroma

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Perniosis

Pityriasis alba

Phytophotodermatitis (to lime juice)

Port wine stain

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Sporotrichosis

Steroid atrophy

Subungal hemorrhage

Twenty Nail dystrophy

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199 Index A Abbreviations, 173–175 Abscess, 3 Acanthosis nigricans, 52–53 Acne vulgaris, 53–57 Acrochordon, 149–150 Acrodermatitis enteropathica, 21 Acromegaly, 20 Acronyms, 173–175 Actinic keratosis, 57–58 Addison’s disease, 20 Aging, 27–28 Allergic contact dermatitis, 79–80 Alopecia, 58–62 Alopecia areata, 24, 61 Amyloidosis, 191 Androgenetic alopecia, 62 Angiofibroma, 191 Angioma, 64–65 Angular cheilitis, 65–66 Annular lesion, 3 Aphthous ulcers, 66–67 Atopic dermatitis (eczema), 67–70 Atrophie blanche, 191 Atrophy, 3 Atypical nevi, 124 Autoimmune disorders, 30 Azure lunula, 23 B Basal cell carcinoma, 70–71 Beau’s lines, 22, 23 Becker nevus, 191 Biopsy, 8–11, 43 Blister, 3

Bruise, 4 Bulla, 3 Bullous pemphigoid, 71–72 Burn, 192 Burrow, 3 C Callus, 192 Candidiasis, 73–74 Canker sores, 66–67 Carbuncle, 3 Cellulitis, 74–75 Cherry angioma, 64–65 Chickenpox, 75–76 Chondrodermatitis nodularis helicis, 77 Cicatrix, 6 Clark’s nevi, 124 Clubbing, 23 Comedo, 3 Congenital nevi, 124 Contact dermatitis, 78–80 Cream, 32 Crust, 3 Cryotherapy, 42 Cushing’s syndrome, 20 Cutaneous horn, 4, 81 Cuti rhomboidalis nuchae, 192 Cysts, 3, 82 D Darier’s disease, 24 Decubitus ulcer, 164–165 Dermatitis contact, 78–80 perioral, 130 seborrheic, 147–148 stasis, 152–153

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TOOLS Dermatitis herpetiformis, 21 Dermatofibroma, 83 Dermatoheliosis, 192 Dermatomyositis, 84–85 Dermatophyte infections, 159–165 Dermatoses, 15–17 Dermis, 7, 8 Dermoscopy, 11 Diabetes mellitus, 21 Diagnostic hints, 17–18 Diascopy, 11 Drugs cutaneous reactions to, 25–27 in pregnancy, 38–41 Dyshidrotic eczema, 193 Dysplastic nevi, 124

Erythroderma, 90–91 Excoriation, 4 Exudate, 4 F Female pattern baldness, 62 Fissure, 4 Fixed drug eruption, 193 Foam, 32 Folliculitis, 4, 92–93 Freckles, 124 Furuncle, 4 G Gardner’s syndrome, 21 Gastrointestinal diseases, 21 Gel, 32 Graft versus host disease, 194 Granuloma, pyogenic, 138–139 Granuloma annulare, 94

E Ecchymosis, 4 Eczema, 21, 24 atopic, 67–70 nummular, 85–87 Electromagnetic spectrum, 44 Elephantiasis nostra verrucosum, 193 Emergencies, 30–31 Endocrine diseases, 20–21 English-Spanish vocabulary, 175–182 Ephelides, 124 Epidermis, 7, 8 Epidermoid cyst, 82 Erosio interdigitalis blastomycetica, 193 Erosion, 4 Erysipelas, 87–88 Erythema, 4 Erythema multiforme, 88–89 Erythema nodosum, 89–90

H Hailey-Hailey disease, 194 Hair growth, 59 Hair loss, 58–62 Half-and-half nails, 23 Halo nevus,194 Hand, foot, and mouth disease, 95 Hemangioma, 96–97 Henoch-Schönlein purpura, 97–98 Herpes simplex virus, 98–100 Herpes zoster virus, 100–101 Hidradenitis suppurativa, 102–103 History, 1 Hives, 7, 166–167 Horn, 4, 81 Hyperhidrosis, 103–104 Hyperlipidemia, 21

200

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201 Hyperthyroidism, 21 Hypothyroidism, 21 I Immunofluorescence test, 11–12 Impetigo, 104–105 Infantile hemangioma, 96–97 Infection, 30 Inflammation, 30 Irritant contact dermatitis, 78–79 Itch, 19–20 J Juvenile xanthogranulomas, 194 K Keratin, 4 Keratoacanthoma, 105–106 Keratosis actinic, 57–58 seborrheic, 148–149 solar, 57–58 Keratosis pilaris, 106–107 Koebnerization, 195 KOH (potassium hydroxide) test, 12 Koilonychia, 23 L Laser therapy, 48–51 Leg ulcer, 162–164 Leichmaniasis, 195 Lentigines, 124 Leprosy, 195 Lesions, 2 Leukocytoclastic vasculitis, 167–168 Lice, 127–128 Lichen amyloidosis, 195

Lichen planus, 24, 107–109 Lichen sclerosus, 109–110 Lichenification, 4 Linear epidermal nevus, 196 Linear lesion, 5 Lipodermatosclerosis, 196 Lipoma, 110–111 Livedo, 5 Liver disease, 21 Liver spots, 124 Longitudinal nail striations, 23 Lotion, 32 Lupus erythematosus, 111–113 Lymphoma, 114–115 M Macule, 5 Male pattern baldness, 62 Mees’ lines, 22, 24 Melanocytic nevi, 123 Melanoma, 116–120 Melasma, 120–121 Moles, 123 Molluscum contagiosum, 121–122 Muehrcke’s lines, 22, 24 Mycosis fungoides, 115 N Nails, 22–24 Neurofibromatosis, 21 Nevi, 123–125 Nikolsky sign, 154 Nodule, 5 Nummular eczema, 85–87 O Ointment, 32 Onycholysis, 23 Onychomycosis, 125–126

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TOOLS P Palmoplanter keratoderma, 196 Papillomatous lesion, 7 Papule, 5 Paronychia, 126–127 Paste, 32 Patch, 5 Patch testing, 12–14 Pediculosis, 127–128 Pellagra, 21 Pemphigus vulgaris, 128–129 Perioral (periorificial) dermatitis, 130 Periungal fibroma, 196 Perniosis, 197 Petechiae, 5 Peutz-Jeghers syndrome, 21 Photobiology, 44–47 Photocarcinogenesis, 46 Phototherapy, 44–47 Phytophotodermatitis, 197 Pigmentation changes, 25, 28 Pitting, 22, 23 Pityriasis alba, 197 Pityriasis rosea, 131 Pityriasis rubra pilaris, 24 Pityriasis versicolor, 132–133 Plaque, 5 Porphyria, 21 Port wine stain, 197 Powder, 32 Pregnancy, 28–29 drugs in, 38–41 Pressure ulcer, 164–165 Pruritus, 19–20 Psoriasis, 24, 133–137 Purpura, 5 Pustule, 5

Pyoderma gangrenosum, 21, 137–138 Pyogenic granuloma, 138–139 R Renal failure, 20 Reticulate lesion, 5 Rosacea, 139–140 S Sarcoidosis, 21, 141–142 Scab, 3 Scabies, 142–143 Scale, 6 Scar, 6, 144–146 Scleroderma, 24 Sclerosis, 6 Scurvy, 21 Sebaceous hyperplasia, 146 Seborrheic dermatitis, 147–148 Seborrheic keratosis, 148–149 Serpiginous lesions, 6 Shingles, 100–101 Skin prototypes, 45 Skin tag, 149–150 Solar keratosis, 57–58 Solar lentigines, 124 Solution, 32 Spanish-English vocabulary, 175–182 Spitz nevus, 124 Splinter hemorrhage, 24 Sporotrichosis, 198 Squamous cell carcinoma, 150–151 Stasis dermatitis, 152–153 Stellate lesion, 6 Steroid atrophy, 198 Steroids, 33–37

202

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203 Stevens-Johnson syndrome, 153–154 Stomatitis, aphthous, 66–67 Strawberry hemangioma, 96–97 Stretch marks, 155–156 Striae, 155–156 Subungal hemorrhage, 198 Surgery, 37–38 Synonyms, 183–187 Syphilis, 156–158 Systemic disease, 20–21 T Target lesions, 6 Telangiectasia, 6, 24 Telogen effluvium, 63 Terminology, 3–7 Terry’s nails, 24 Tinea, 159–165 Tinea capitis, 161 Tinea corporis, 160 Tinea cruris, 161 Tinea pedis, 160 Tinea unguium, 125–126 Tinea versicolor, 132–133 Topical steroids, 33–37 Toxic epidermal necrolysis (TEN), 153–154 Trichotillomania, 63–64

Tuberous sclerosis, 21 Twenty nail dystrophy, 198 Tzanck smear, 14 U Ulcer, 6 aphthous, 66–67 leg, 162–164 pressure, 164–165 Umbilicated lesion, 6 Urticaria, 166–167 V Varicella, 75–76 Vasculitis, 167–168 Verrucae, 171–172 Vesicle, 7 Vesiculobullous disorders, 30 Vitiligo, 169–170 W Warts, 7, 171–172 Websites, 188–190 Wheal, 7 Whorled lesion, 7 Wood’s lamp, 14 Y Yellow nail, 23

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